Compounds or agents that combine with cyclooxygenase (PROSTAGLANDIN-ENDOPEROXIDE SYNTHASES) and thereby prevent its substrate-enzyme combination with arachidonic acid and the formation of eicosanoids, prostaglandins, and thromboxanes.
An inducibly-expressed subtype of prostaglandin-endoperoxide synthase. It plays an important role in many cellular processes and INFLAMMATION. It is the target of COX2 INHIBITORS.
A constitutively-expressed subtype of prostaglandin-endoperoxide synthase. It plays an important role in many cellular processes.
A non-steroidal anti-inflammatory agent (NSAID) that inhibits the enzyme cyclooxygenase necessary for the formation of prostaglandins and other autacoids. It also inhibits the motility of polymorphonuclear leukocytes.
A subclass of cyclooxygenase inhibitors with specificity for CYCLOOXYGENASE-2.
Enzyme complexes that catalyze the formation of PROSTAGLANDINS from the appropriate unsaturated FATTY ACIDS, molecular OXYGEN, and a reduced acceptor.
The most common and most biologically active of the mammalian prostaglandins. It exhibits most biological activities characteristic of prostaglandins and has been used extensively as an oxytocic agent. The compound also displays a protective effect on the intestinal mucosa.
A group of compounds derived from unsaturated 20-carbon fatty acids, primarily arachidonic acid, via the cyclooxygenase pathway. They are extremely potent mediators of a diverse group of physiological processes.
Compounds that bind to and inhibit that enzymatic activity of LIPOXYGENASES. Included under this category are inhibitors that are specific for lipoxygenase subtypes and act to reduce the production of LEUKOTRIENES.
A nonsteroidal anti-inflammatory agent with analgesic properties used in the therapy of rheumatism and arthritis.
An unsaturated, essential fatty acid. It is found in animal and human fat as well as in the liver, brain, and glandular organs, and is a constituent of animal phosphatides. It is formed by the synthesis from dietary linoleic acid and is a precursor in the biosynthesis of prostaglandins, thromboxanes, and leukotrienes.
A cyclooxygenase inhibiting, non-steroidal anti-inflammatory agent (NSAID) that is well established in treating rheumatoid arthritis and osteoarthritis and used for musculoskeletal disorders, dysmenorrhea, and postoperative pain. Its long half-life enables it to be administered once daily.
A potent lipoxygenase inhibitor that interferes with arachidonic acid metabolism. The compound also inhibits formyltetrahydrofolate synthetase, carboxylesterase, and cyclooxygenase to a lesser extent. It also serves as an antioxidant in fats and oils.
An anti-inflammatory analgesic and antipyretic of the phenylalkynoic acid series. It has been shown to reduce bone resorption in periodontal disease by inhibiting CARBONIC ANHYDRASE.
Anti-inflammatory agents that are non-steroidal in nature. In addition to anti-inflammatory actions, they have analgesic, antipyretic, and platelet-inhibitory actions.They act by blocking the synthesis of prostaglandins by inhibiting cyclooxygenase, which converts arachidonic acid to cyclic endoperoxides, precursors of prostaglandins. Inhibition of prostaglandin synthesis accounts for their analgesic, antipyretic, and platelet-inhibitory actions; other mechanisms may contribute to their anti-inflammatory effects.
A non-steroidal anti-inflammatory agent with antipyretic and antigranulation activities. It also inhibits prostaglandin biosynthesis.
A non-steroidal anti-inflammatory agent (NSAID) with antipyretic and analgesic actions. It is primarily available as the sodium salt.
A stable, physiologically active compound formed in vivo from the prostaglandin endoperoxides. It is important in the platelet-release reaction (release of ADP and serotonin).
An enzyme of the oxidoreductase class primarily found in PLANTS. It catalyzes reactions between linoleate and other fatty acids and oxygen to form hydroperoxy-fatty acid derivatives.
Structurally related forms of an enzyme. Each isoenzyme has the same mechanism and classification, but differs in its chemical, physical, or immunological characteristics.
Azoles of two nitrogens at the 1,2 positions, next to each other, in contrast with IMIDAZOLES in which they are at the 1,3 positions.
A group of compounds that contain the structure SO2NH2.
The prototypical analgesic used in the treatment of mild to moderate pain. It has anti-inflammatory and antipyretic properties and acts as an inhibitor of cyclooxygenase which results in the inhibition of the biosynthesis of prostaglandins. Aspirin also inhibits platelet aggregation and is used in the prevention of arterial and venous thrombosis. (From Martindale, The Extra Pharmacopoeia, 30th ed, p5)
The physiologically active and stable hydrolysis product of EPOPROSTENOL. Found in nearly all mammalian tissue.
A class of compounds named after and generally derived from C20 fatty acids (EICOSANOIC ACIDS) that includes PROSTAGLANDINS; LEUKOTRIENES; THROMBOXANES, and HYDROXYEICOSATETRAENOIC ACIDS. They have hormone-like effects mediated by specialized receptors (RECEPTORS, EICOSANOID).
A 20-carbon unsaturated fatty acid containing 4 alkyne bonds. It inhibits the enzymatic conversion of arachidonic acid to prostaglandins E(2) and F(2a).
A non-steroidal anti-inflammatory agent (ANTI-INFLAMMATORY AGENTS, NON-STEROIDAL) similar in mode of action to INDOMETHACIN.
A dual inhibitor of both cyclooxygenase and lipoxygenase pathways. It exerts an anti-inflammatory effect by inhibiting the formation of prostaglandins and leukotrienes. The drug also enhances pulmonary hypoxic vasoconstriction and has a protective effect after myocardial ischemia.
A prostaglandin that is a powerful vasodilator and inhibits platelet aggregation. It is biosynthesized enzymatically from PROSTAGLANDIN ENDOPEROXIDES in human vascular tissue. The sodium salt has been also used to treat primary pulmonary hypertension (HYPERTENSION, PULMONARY).
An unstable intermediate between the prostaglandin endoperoxides and thromboxane B2. The compound has a bicyclic oxaneoxetane structure. It is a potent inducer of platelet aggregation and causes vasoconstriction. It is the principal component of rabbit aorta contracting substance (RCS).
The physiological widening of BLOOD VESSELS by relaxing the underlying VASCULAR SMOOTH MUSCLE.
Cell surface receptors which bind prostaglandins with a high affinity and trigger intracellular changes which influence the behavior of cells. Prostaglandin E receptors prefer prostaglandin E2 to other endogenous prostaglandins. They are subdivided into EP1, EP2, and EP3 types based on their effects and their pharmacology.
(11 alpha,13E,15S)-11,15-Dihydroxy-9-oxoprost-13-en-1-oic acid (PGE(1)); (5Z,11 alpha,13E,15S)-11,15-dihydroxy-9-oxoprosta-5,13-dien-1-oic acid (PGE(2)); and (5Z,11 alpha,13E,15S,17Z)-11,15-dihydroxy-9-oxoprosta-5,13,17-trien-1-oic acid (PGE(3)). Three of the six naturally occurring prostaglandins. They are considered primary in that no one is derived from another in living organisms. Originally isolated from sheep seminal fluid and vesicles, they are found in many organs and tissues and play a major role in mediating various physiological activities.
An enzyme found predominantly in platelet microsomes. It catalyzes the conversion of PGG(2) and PGH(2) (prostaglandin endoperoxides) to thromboxane A2. EC
Physiologically active compounds found in many organs of the body. They are formed in vivo from the prostaglandin endoperoxides and cause platelet aggregation, contraction of arteries, and other biological effects. Thromboxanes are important mediators of the actions of polyunsaturated fatty acids transformed by cyclooxygenase.
A nonapeptide messenger that is enzymatically produced from KALLIDIN in the blood where it is a potent but short-lived agent of arteriolar dilation and increased capillary permeability. Bradykinin is also released from MAST CELLS during asthma attacks, from gut walls as a gastrointestinal vasodilator, from damaged tissues as a pain signal, and may be a neurotransmitter.
An anti-inflammatory agent with analgesic and antipyretic properties. Both the acid and its sodium salt are used in the treatment of rheumatoid arthritis and other rheumatic or musculoskeletal disorders, dysmenorrhea, and acute gout.
A naturally occurring prostaglandin that has oxytocic, luteolytic, and abortifacient activities. Due to its vasocontractile properties, the compound has a variety of other biological actions.
A non-selective inhibitor of nitric oxide synthase. It has been used experimentally to induce hypertension.
A family of biologically active compounds derived from arachidonic acid by oxidative metabolism through the 5-lipoxygenase pathway. They participate in host defense reactions and pathophysiological conditions such as immediate hypersensitivity and inflammation. They have potent actions on many essential organs and systems, including the cardiovascular, pulmonary, and central nervous system as well as the gastrointestinal tract and the immune system.
Eicosatetraenoic acids substituted in any position by one or more hydroxy groups. They are important intermediates in a series of biosynthetic processes leading from arachidonic acid to a number of biologically active compounds such as prostaglandins, thromboxanes, and leukotrienes.
A free radical gas produced endogenously by a variety of mammalian cells, synthesized from ARGININE by NITRIC OXIDE SYNTHASE. Nitric oxide is one of the ENDOTHELIUM-DEPENDENT RELAXING FACTORS released by the vascular endothelium and mediates VASODILATION. It also inhibits platelet aggregation, induces disaggregation of aggregated platelets, and inhibits platelet adhesion to the vascular endothelium. Nitric oxide activates cytosolic GUANYLATE CYCLASE and thus elevates intracellular levels of CYCLIC GMP.
The relationship between the dose of an administered drug and the response of the organism to the drug.
An enzyme that catalyzes the oxidation of arachidonic acid to yield 5-hydroperoxyarachidonate (5-HPETE) which is rapidly converted by a peroxidase to 5-hydroxy-6,8,11,14-eicosatetraenoate (5-HETE). The 5-hydroperoxides are preferentially formed in leukocytes.
A 20-carbon-chain fatty acid, unsaturated at positions 8, 11, and 14. It differs from arachidonic acid, 5,8,11,14-eicosatetraenoic acid, only at position 5.
A drug that has analgesic and anti-inflammatory properties. Following reports of adverse reactions including reports of carcinogenicity in animal studies it was withdrawn from the market worldwide. (From Martindale, The Extra Pharmacopoeia, 30th ed, p21)
A pyrrolizine carboxylic acid derivative structurally related to INDOMETHACIN. It is an NSAID and is used principally for its analgesic activity. (From Martindale The Extra Pharmacopoeia, 31st ed)
The physiological narrowing of BLOOD VESSELS by contraction of the VASCULAR SMOOTH MUSCLE.
An acridine derivative formerly widely used as an antimalarial but superseded by chloroquine in recent years. It has also been used as an anthelmintic and in the treatment of giardiasis and malignant effusions. It is used in cell biological experiments as an inhibitor of phospholipase A2.
A sulfinylindene derivative prodrug whose sulfinyl moiety is converted in vivo to an active NSAID analgesic. Specifically, the prodrug is converted by liver enzymes to a sulfide which is excreted in the bile and then reabsorbed from the intestine. This helps to maintain constant blood levels with reduced gastrointestinal side effects.
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
Compounds that inhibit the action of prostaglandins.
Enzymes catalyzing the oxidation of arachidonic acid to hydroperoxyarachidonates. These products are then rapidly converted by a peroxidase to hydroxyeicosatetraenoic acids. The positional specificity of the enzyme reaction varies from tissue to tissue. The final lipoxygenase pathway leads to the leukotrienes. EC 1.13.11.- .
A potent vasodilator agent that increases peripheral blood flow.
Phospholipases that hydrolyze one of the acyl groups of phosphoglycerides or glycerophosphatidates.
Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components.
Proteins which are found in membranes including cellular and intracellular membranes. They consist of two types, peripheral and integral proteins. They include most membrane-associated enzymes, antigenic proteins, transport proteins, and drug, hormone, and lectin receptors.
An IBUPROFEN-type anti-inflammatory analgesic and antipyretic. It is used in the treatment of rheumatoid arthritis and osteoarthritis.
An NADPH-dependent enzyme that catalyzes the conversion of L-ARGININE and OXYGEN to produce CITRULLINE and NITRIC OXIDE.
Endogenously-synthesized compounds that influence biological processes not otherwise classified under ENZYMES; HORMONES or HORMONE ANTAGONISTS.
The major metabolite in neutrophil polymorphonuclear leukocytes. It stimulates polymorphonuclear cell function (degranulation, formation of oxygen-centered free radicals, arachidonic acid release, and metabolism). (From Dictionary of Prostaglandins and Related Compounds, 1990)
Phospholipases that hydrolyze the acyl group attached to the 2-position of PHOSPHOGLYCERIDES.
Paracrine substances produced by the VASCULAR ENDOTHELIUM with VASCULAR SMOOTH MUSCLE relaxation (VASODILATION) activities. Several factors have been identified, including NITRIC OXIDE and PROSTACYCLIN.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
A neurotransmitter found at neuromuscular junctions, autonomic ganglia, parasympathetic effector junctions, a subset of sympathetic effector junctions, and at many sites in the central nervous system.
Cell surface proteins that bind THROMBOXANES with high affinity and trigger intracellular changes influencing the behavior of cells. Some thromboxane receptors act via the inositol phosphate and diacylglycerol second messenger systems.
A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.
Drugs used to cause dilation of the blood vessels.
Drugs used to cause constriction of the blood vessels.
An ionophorous, polyether antibiotic from Streptomyces chartreusensis. It binds and transports CALCIUM and other divalent cations across membranes and uncouples oxidative phosphorylation while inhibiting ATPase of rat liver mitochondria. The substance is used mostly as a biochemical tool to study the role of divalent cations in various biological systems.
The smallest divisions of the arteries located between the muscular arteries and the capillaries.
A stable prostaglandin endoperoxide analog which serves as a thromboxane mimetic. Its actions include mimicking the hydro-osmotic effect of VASOPRESSIN and activation of TYPE C PHOSPHOLIPASES. (From J Pharmacol Exp Ther 1983;224(1): 108-117; Biochem J 1984;222(1):103-110)
Cyclic esters of hydroxy carboxylic acids, containing a 1-oxacycloalkan-2-one structure. Large cyclic lactones of over a dozen atoms are MACROLIDES.
The principal cyclooxygenase metabolite of arachidonic acid. It is released upon activation of mast cells and is also synthesized by alveolar macrophages. Among its many biological actions, the most important are its bronchoconstrictor, platelet-activating-factor-inhibitory, and cytotoxic effects.
An inhibitor of nitric oxide synthetase which has been shown to prevent glutamate toxicity. Nitroarginine has been experimentally tested for its ability to prevent ammonia toxicity and ammonia-induced alterations in brain energy and ammonia metabolites. (Neurochem Res 1995:200(4):451-6)
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
A subtype of prostaglandin E receptors that specifically couples to GS ALPHA GTP-BINDING PROTEIN SUBUNITS and subsequently activates ADENYLYL CYCLASES.
A subtype of prostaglandin E receptors that specifically couples to GS ALPHA GTP-BINDING PROTEIN SUBUNITS and subsequently activates ADENYLYL CYCLASES. The receptor may also signal through the activation of PHOSPHATIDYLINOSITOL 3-KINASE.
A group of LEUKOTRIENES; (LTC4; LTD4; and LTE4) that is the major mediator of BRONCHOCONSTRICTION; HYPERSENSITIVITY; and other allergic reactions. Earlier studies described a "slow-reacting substance of ANAPHYLAXIS" released from lung by cobra venom or after anaphylactic shock. The relationship between SRS-A leukotrienes was established by UV which showed the presence of the conjugated triene. (From Merck Index, 11th ed)
(9 alpha,11 alpha,13E,15S)-9,11,15-Trihydroxyprost-13-en-1-oic acid (PGF(1 alpha)); (5Z,9 alpha,11,alpha,13E,15S)-9,11,15-trihydroxyprosta-5,13-dien-1-oic acid (PGF(2 alpha)); (5Z,9 alpha,11 alpha,13E,15S,17Z)-9,11,15-trihydroxyprosta-5,13,17-trien-1-oic acid (PGF(3 alpha)). A family of prostaglandins that includes three of the six naturally occurring prostaglandins. All naturally occurring PGF have an alpha configuration at the 9-carbon position. They stimulate uterine and bronchial smooth muscle and are often used as oxytocics.
Analogs or derivatives of prostaglandins E that do not occur naturally in the body. They do not include the product of the chemical synthesis of hormonal PGE.
The nonstriated involuntary muscle tissue of blood vessels.
Arteries which arise from the abdominal aorta and distribute to most of the intestines.
A phospholipid derivative formed by PLATELETS; BASOPHILS; NEUTROPHILS; MONOCYTES; and MACROPHAGES. It is a potent platelet aggregating agent and inducer of systemic anaphylactic symptoms, including HYPOTENSION; THROMBOCYTOPENIA; NEUTROPENIA; and BRONCHOCONSTRICTION.
Non-nucleated disk-shaped cells formed in the megakaryocyte and found in the blood of all mammals. They are mainly involved in blood coagulation.
The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.
The attachment of PLATELETS to one another. This clumping together can be induced by a number of agents (e.g., THROMBIN; COLLAGEN) and is part of the mechanism leading to the formation of a THROMBUS.
The innermost layer of the three meninges covering the brain and spinal cord. It is the fine vascular membrane that lies under the ARACHNOID and the DURA MATER.
A powerful vasodilator used in emergencies to lower blood pressure or to improve cardiac function. It is also an indicator for free sulfhydryl groups in proteins.
A group of 1,2-benzenediols that contain the general formula R-C6H5O2.
The domestic dog, Canis familiaris, comprising about 400 breeds, of the carnivore family CANIDAE. They are worldwide in distribution and live in association with people. (Walker's Mammals of the World, 5th ed, p1065)
A soluble factor produced by MONOCYTES; MACROPHAGES, and other cells which activates T-lymphocytes and potentiates their response to mitogens or antigens. Interleukin-1 is a general term refers to either of the two distinct proteins, INTERLEUKIN-1ALPHA and INTERLEUKIN-1BETA. The biological effects of IL-1 include the ability to replace macrophage requirements for T-cell activation.
A competitive inhibitor of nitric oxide synthetase.
The action of a drug that may affect the activity, metabolism, or toxicity of another drug.
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.
A subclass of analgesic agents that typically do not bind to OPIOID RECEPTORS and are not addictive. Many non-narcotic analgesics are offered as NONPRESCRIPTION DRUGS.
A class of enzymes that catalyze the hydrolysis of phosphoglycerides or glycerophosphatidates. EC 3.1.-.
A doubly unsaturated fatty acid, occurring widely in plant glycosides. It is an essential fatty acid in mammalian nutrition and is used in the biosynthesis of prostaglandins and cell membranes. (From Stedman, 26th ed)
Cell surface receptors that bind BRADYKININ and related KININS with high affinity and trigger intracellular changes which influence the behavior of cells. The identified receptor types (B-1 and B-2, or BK-1 and BK-2) recognize endogenous KALLIDIN; t-kinins; and certain bradykinin fragments as well as bradykinin itself.
FATTY ACIDS in which the carbon chain contains one or more double or triple carbon-carbon bonds.
Lipid-containing polysaccharides which are endotoxins and important group-specific antigens. They are often derived from the cell wall of gram-negative bacteria and induce immunoglobulin secretion. The lipopolysaccharide molecule consists of three parts: LIPID A, core polysaccharide, and O-specific chains (O ANTIGENS). When derived from Escherichia coli, lipopolysaccharides serve as polyclonal B-cell mitogens commonly used in laboratory immunology. (From Dorland, 28th ed)
The force that opposes the flow of BLOOD through a vascular bed. It is equal to the difference in BLOOD PRESSURE across the vascular bed divided by the CARDIAC OUTPUT.
Elements of limited time intervals, contributing to particular results or situations.
Enzymes of the isomerase class that catalyze the oxidation of one part of a molecule with a corresponding reduction of another part of the same molecule. They include enzymes converting aldoses to ketoses (ALDOSE-KETOSE ISOMERASES), enzymes shifting a carbon-carbon double bond (CARBON-CARBON DOUBLE BOND ISOMERASES), and enzymes transposing S-S bonds (SULFUR-SULFUR BOND ISOMERASES). (From Enzyme Nomenclature, 1992) EC 5.3.
Analgesic antipyretic derivative of acetanilide. It has weak anti-inflammatory properties and is used as a common analgesic, but may cause liver, blood cell, and kidney damage.
Acrylic acids or acrylates which are substituted in the C-2 position with a methyl group.
Any of the ruminant mammals with curved horns in the genus Ovis, family Bovidae. They possess lachrymal grooves and interdigital glands, which are absent in GOATS.
Highly reactive molecules with an unsatisfied electron valence pair. Free radicals are produced in both normal and pathological processes. They are proven or suspected agents of tissue damage in a wide variety of circumstances including radiation, damage from environment chemicals, and aging. Natural and pharmacological prevention of free radical damage is being actively investigated.
A process leading to shortening and/or development of tension in muscle tissue. Muscle contraction occurs by a sliding filament mechanism whereby actin filaments slide inward among the myosin filaments.
A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes.
Eighteen-carbon essential fatty acids that contain two double bonds.
A common name used for the genus Cavia. The most common species is Cavia porcellus which is the domesticated guinea pig used for pets and biomedical research.
The flow of BLOOD through or around an organ or region of the body.
An alkylamide found in CAPSICUM that acts at TRPV CATION CHANNELS.
Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations or by parent x offspring matings carried out with certain restrictions. This also includes animals with a long history of closed colony breeding.
A group of physiologically active prostaglandin endoperoxides. They are precursors in the biosynthesis of prostaglandins and thromboxanes. Most frequently encountered member of this group is the prostaglandin G2.
Lining of the STOMACH, consisting of an inner EPITHELIUM, a middle LAMINA PROPRIA, and an outer MUSCULARIS MUCOSAE. The surface cells produce MUCUS that protects the stomach from attack by digestive acid and enzymes. When the epithelium invaginates into the LAMINA PROPRIA at various region of the stomach (CARDIA; GASTRIC FUNDUS; and PYLORUS), different tubular gastric glands are formed. These glands consist of cells that secrete mucus, enzymes, HYDROCHLORIC ACID, or hormones.
An essential amino acid that is physiologically active in the L-form.
Any of various animals that constitute the family Suidae and comprise stout-bodied, short-legged omnivorous mammals with thick skin, usually covered with coarse bristles, a rather long mobile snout, and small tail. Included are the genera Babyrousa, Phacochoerus (wart hogs), and Sus, the latter containing the domestic pig (see SUS SCROFA).
A class of drugs that act by inhibition of potassium efflux through cell membranes. Blockade of potassium channels prolongs the duration of ACTION POTENTIALS. They are used as ANTI-ARRHYTHMIA AGENTS and VASODILATOR AGENTS.
That phase of a muscle twitch during which a muscle returns to a resting position.
An adenine nucleotide containing one phosphate group which is esterified to both the 3'- and 5'-positions of the sugar moiety. It is a second messenger and a key intracellular regulator, functioning as a mediator of activity for a number of hormones, including epinephrine, glucagon, and ACTH.
An abnormal elevation of body temperature, usually as a result of a pathologic process.
A saclike, glandular diverticulum on each ductus deferens in male vertebrates. It is united with the excretory duct and serves for temporary storage of semen. (From McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)
Treatment process involving the injection of fluid into an organ or tissue.
Either of the pair of organs occupying the cavity of the thorax that effect the aeration of the blood.
Unstriated and unstriped muscle, one of the muscles of the internal organs, blood vessels, hair follicles, etc. Contractile elements are elongated, usually spindle-shaped cells with centrally located nuclei. Smooth muscle fibers are bound together into sheets or bundles by reticular fibers and frequently elastic nets are also abundant. (From Stedman, 25th ed)
An amine derived by enzymatic decarboxylation of HISTIDINE. It is a powerful stimulant of gastric secretion, a constrictor of bronchial smooth muscle, a vasodilator, and also a centrally acting neurotransmitter.
The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.
The fission of a CELL. It includes CYTOKINESIS, when the CYTOPLASM of a cell is divided, and CELL NUCLEUS DIVISION.
A superfamily of hundreds of closely related HEMEPROTEINS found throughout the phylogenetic spectrum, from animals, plants, fungi, to bacteria. They include numerous complex monooxygenases (MIXED FUNCTION OXYGENASES). In animals, these P-450 enzymes serve two major functions: (1) biosynthesis of steroids, fatty acids, and bile acids; (2) metabolism of endogenous and a wide variety of exogenous substrates, such as toxins and drugs (BIOTRANSFORMATION). They are classified, according to their sequence similarities rather than functions, into CYP gene families (>40% homology) and subfamilies (>59% homology). For example, enzymes from the CYP1, CYP2, and CYP3 gene families are responsible for most drug metabolism.
The veins and arteries of the HEART.
Compounds containing 1,3-diazole, a five membered aromatic ring containing two nitrogen atoms separated by one of the carbons. Chemically reduced ones include IMIDAZOLINES and IMIDAZOLIDINES. Distinguish from 1,2-diazole (PYRAZOLES).
An alpha-1 adrenergic agonist used as a mydriatic, nasal decongestant, and cardiotonic agent.
The main trunk of the systemic arteries.
Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.
Precursor of epinephrine that is secreted by the adrenal medulla and is a widespread central and autonomic neurotransmitter. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers and of the diffuse projection system in the brain arising from the locus ceruleus. It is also found in plants and is used pharmacologically as a sympathomimetic.
A layer of epithelium that lines the heart, blood vessels (ENDOTHELIUM, VASCULAR), lymph vessels (ENDOTHELIUM, LYMPHATIC), and the serous cavities of the body.
The action of a drug in promoting or enhancing the effectiveness of another drug.
The portion of the descending aorta proceeding from the arch of the aorta and extending to the DIAPHRAGM, eventually connecting to the ABDOMINAL AORTA.
The relatively long-lived phagocytic cell of mammalian tissues that are derived from blood MONOCYTES. Main types are PERITONEAL MACROPHAGES; ALVEOLAR MACROPHAGES; HISTIOCYTES; KUPFFER CELLS of the liver; and OSTEOCLASTS. They may further differentiate within chronic inflammatory lesions to EPITHELIOID CELLS or may fuse to form FOREIGN BODY GIANT CELLS or LANGHANS GIANT CELLS. (from The Dictionary of Cell Biology, Lackie and Dow, 3rd ed.)
Compounds with a six membered aromatic ring containing NITROGEN. The saturated version is PIPERIDINES.
Serum glycoprotein produced by activated MACROPHAGES and other mammalian MONONUCLEAR LEUKOCYTES. It has necrotizing activity against tumor cell lines and increases ability to reject tumor transplants. Also known as TNF-alpha, it is only 30% homologous to TNF-beta (LYMPHOTOXIN), but they share TNF RECEPTORS.
The rate dynamics in chemical or physical systems.
Established cell cultures that have the potential to propagate indefinitely.
The short wide vessel arising from the conus arteriosus of the right ventricle and conveying unaerated blood to the lungs.
A CALCIUM-dependent, constitutively-expressed form of nitric oxide synthase found primarily in ENDOTHELIAL CELLS.
An antidiabetic sulfonylurea derivative with actions similar to those of chlorpropamide.
Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.
Benzopyrroles with the nitrogen at the number one carbon adjacent to the benzyl portion, in contrast to ISOINDOLES which have the nitrogen away from the six-membered ring.
Guanosine cyclic 3',5'-(hydrogen phosphate). A guanine nucleotide containing one phosphate group which is esterified to the sugar moiety in both the 3'- and 5'-positions. It is a cellular regulatory agent and has been described as a second messenger. Its levels increase in response to a variety of hormones, including acetylcholine, insulin, and oxytocin and it has been found to activate specific protein kinases. (From Merck Index, 11th ed)
An octapeptide that is a potent but labile vasoconstrictor. It is produced from angiotensin I after the removal of two amino acids at the C-terminal by ANGIOTENSIN CONVERTING ENZYME. The amino acid in position 5 varies in different species. To block VASOCONSTRICTION and HYPERTENSION effect of angiotensin II, patients are often treated with ACE INHIBITORS or with ANGIOTENSIN II TYPE 1 RECEPTOR BLOCKERS.
A cyclic endoperoxide intermediate produced by the action of CYCLOOXYGENASE on ARACHIDONIC ACID. It is further converted by a series of specific enzymes to the series 2 prostaglandins.
An increase in the rate of synthesis of an enzyme due to the presence of an inducer which acts to derepress the gene responsible for enzyme synthesis.
The movement and the forces involved in the movement of the blood through the CARDIOVASCULAR SYSTEM.
Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in enzyme synthesis.
Conversion of an inactive form of an enzyme to one possessing metabolic activity. It includes 1, activation by ions (activators); 2, activation by cofactors (coenzymes); and 3, conversion of an enzyme precursor (proenzyme or zymogen) to an active enzyme.
Liquid chromatographic techniques which feature high inlet pressures, high sensitivity, and high speed.
The vessels carrying blood away from the heart.
Highly reactive compounds produced when oxygen is reduced by a single electron. In biological systems, they may be generated during the normal catalytic function of a number of enzymes and during the oxidation of hemoglobin to METHEMOGLOBIN. In living organisms, SUPEROXIDE DISMUTASE protects the cell from the deleterious effects of superoxides.
A biochemical messenger and regulator, synthesized from the essential amino acid L-TRYPTOPHAN. In humans it is found primarily in the central nervous system, gastrointestinal tract, and blood platelets. Serotonin mediates several important physiological functions including neurotransmission, gastrointestinal motility, hemostasis, and cardiovascular integrity. Multiple receptor families (RECEPTORS, SEROTONIN) explain the broad physiological actions and distribution of this biochemical mediator.
An enzyme formed from PROTHROMBIN that converts FIBRINOGEN to FIBRIN.
Granular leukocytes having a nucleus with three to five lobes connected by slender threads of chromatin, and cytoplasm containing fine inconspicuous granules and stainable by neutral dyes.
Cells grown in vitro from neoplastic tissue. If they can be established as a TUMOR CELL LINE, they can be propagated in cell culture indefinitely.
Cell membrane glycoproteins that are selectively permeable to potassium ions. At least eight major groups of K channels exist and they are made up of dozens of different subunits.
A subclass of phospholipases that hydrolyze the phosphoester bond found in the third position of GLYCEROPHOSPHOLIPIDS. Although the singular term phospholipase C specifically refers to an enzyme that catalyzes the hydrolysis of PHOSPHATIDYLCHOLINE (EC, it is commonly used in the literature to refer to broad variety of enzymes that specifically catalyze the hydrolysis of PHOSPHATIDYLINOSITOLS.
An oxidoreductase that catalyzes the reaction between superoxide anions and hydrogen to yield molecular oxygen and hydrogen peroxide. The enzyme protects the cell against dangerous levels of superoxide. EC
A subtype of prostaglandin E receptors that specifically couples to GTP-BINDING PROTEIN ALPHA SUBUNIT, GQ and the subsequently activates TYPE C PHOSPHOLIPASES. Additional evidence has shown that the receptor can act through a calcium-dependent signaling pathway.
A group of physiologically active prostaglandin endoperoxides. They are precursors in the biosynthesis of prostaglandins and thromboxanes. The most frequently encountered member of this group is the prostaglandin H2.
One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.
The salts or esters of salicylic acids, or salicylate esters of an organic acid. Some of these have analgesic, antipyretic, and anti-inflammatory activities by inhibiting prostaglandin synthesis.
A CALCIUM-independent subtype of nitric oxide synthase that may play a role in immune function. It is an inducible enzyme whose expression is transcriptionally regulated by a variety of CYTOKINES.
An adenine nucleotide containing three phosphate groups esterified to the sugar moiety. In addition to its crucial roles in metabolism adenosine triphosphate is a neurotransmitter.
Cell surface receptors that bind prostaglandins with high affinity and trigger intracellular changes which influence the behavior of cells. Prostaglandin receptor subtypes have been tentatively named according to their relative affinities for the endogenous prostaglandins. They include those which prefer prostaglandin D2 (DP receptors), prostaglandin E2 (EP1, EP2, and EP3 receptors), prostaglandin F2-alpha (FP receptors), and prostacyclin (IP receptors).
A lipoxygenase metabolite of ARACHIDONIC ACID. It is a highly selective ligand used to label mu-opioid receptors in both membranes and tissue sections. The 12-S-HETE analog has been reported to augment tumor cell metastatic potential through activation of protein kinase C. (J Pharmacol Exp Ther 1995; 274(3):1545-51; J Natl Cancer Inst 1994; 86(15):1145-51)
A pyrrolizine carboxylic acid derivative structurally related to INDOMETHACIN. It is a non-steroidal anti-inflammatory agent used for analgesia for postoperative pain and inhibits cyclooxygenase activity.
A subtype of prostaglandin E receptors that specifically couples to GTP-BINDING PROTEIN ALPHA SUBUNIT, GI and subsequently inhibits ADENYLYL CYCLASES.
A subclass of eicosanoid receptors that have specificity for THROMBOXANE A2 and PROSTAGLANDIN H2.
Artifactual vesicles formed from the endoplasmic reticulum when cells are disrupted. They are isolated by differential centrifugation and are composed of three structural features: rough vesicles, smooth vesicles, and ribosomes. Numerous enzyme activities are associated with the microsomal fraction. (Glick, Glossary of Biochemistry and Molecular Biology, 1990; from Rieger et al., Glossary of Genetics: Classical and Molecular, 5th ed)

Mechanisms of prostaglandin E2 release by intact cells expressing cyclooxygenase-2: evidence for a 'two-component' model. (1/3239)

Prostaglandin (PG) release in cells expressing constitutive cyclooxygenase-1 is known to be regulated by liberation of arachidonic acid by phospholipase A2 followed by metabolism by cyclooxygenase. However, the relative contribution of phospholipase A2 to the release of PGs in cells expressing cyclooxygenase-2 is not clear. We addressed this question by using radioimmunoassay to measure PGE2 release by human cells (A549) induced to express cyclooxygenase-2 (measured by Western blot analysis) by interleukin-1beta. Cells were either unstimulated or stimulated with agents known to activate phospholipase A2 (bradykinin, Des-Arg10-kallidin, or the calcium ionophore A23187) or treated with exogenous arachidonic acid. When cells were treated to express cyclooxygenase-2, the levels of PGE2 released over 15 min were undetectable; however, in the same cells stimulated with bradykinin, A23187, or arachidonic acid, large amounts of prostanoid were produced. Using selective inhibitors/antagonists, we found that the effects of bradykinin were mediated by B2 receptor activation and that prostanoid release was due to cyclooxygenase-2, and not cyclooxygenase-1, activity. In addition, we show that the release of PGE2 stimulated by either bradykinin, A23187, or arachidonic acid was inhibited by the phospholipase A2 inhibitor arachidonate trifluoromethyl ketone. Hence, we have demonstrated that PGE2 is released by two components: induction of cyclooxygenase-2 and supply of substrate, probably via activation of phospholipase A2. This is illustrated in A549 cells by a clear synergy between the cytokine interleukin-1beta and the kinin bradykinin.  (+info)

Inhibition of prostaglandin synthesis up-regulates cyclooxygenase-2 induced by lipopolysaccharide and peroxisomal proliferators. (2/3239)

Primary cultures of fetal hepatocytes expressed cyclooxygenase-2 (COX-2) upon stimulation with bacterial lipopolysaccharide (LPS) or peroxisomal proliferators. This enzyme was active and a good correlation between the mRNA levels, the amount of protein, and the synthesis of prostaglandin E2 was observed. However, when cells were incubated in the presence of indomethacin or the COX-2-specific inhibitor NS398, the amount of COX-2 protein increased 5-fold after activation with LPS and 2-fold after treatment with clofibrate. This up-regulation of COX-2 was not observed at the mRNA level. The mechanism of protein accumulation might involve either a direct stabilization of the enzyme by the inhibitors or the absence of prostaglandins involved in the regulation of its turnover. Among the prostaglandins assayed, only 15-deoxy-Prostaglandin J2 exerted a statistically significant decrease in the COX-2 levels in cells stimulated with LPS or LPS plus NS398. The accumulation of COX-2 in the presence of inhibitors was also observed in peritoneal macrophages treated under identical conditions. These results indicate that COX-2 protein accumulates after enzyme inhibition, and because removal of the inhibitors restored the enzyme activity, suppression of treatment with reversible COX-2 inhibitors may cause a transient overproduction of prostaglandins.  (+info)

Characterization of the analgesic and anti-inflammatory activities of ketorolac and its enantiomers in the rat. (3/3239)

The marked analgesic efficacy of ketorolac in humans, relative to other nonsteroidal anti-inflammatory drugs (NSAIDs), has lead to speculation as to whether additional non-NSAID mechanism(s) contribute to its analgesic actions. To evaluate this possibility, we characterized (R,S)-ketorolac's pharmacological properties in vivo and in vitro using the nonselective cyclooxygenase (COX) inhibitors [indomethacin (INDO) and diclofenac sodium (DS)] as well as the selective COX-2 inhibitor, celecoxib, as references. The potency of racemic (R,S)-ketorolac was similar in tests of acetic acid-induced writhing, carrageenan-induced paw hyperalgesia, and carrageenan-induced edema formation in rats; ID50 values = 0.24, 0. 29, and 0.08 mg/kg, respectively. (R,S)-ketorolac's actions were stereospecific, with (S)-ketorolac possessing the biological activity of the racemate in the above tests. The analgesic potencies for (R,S)-, (S)-, and (R)-ketorolac, INDO, and DS were highly correlated with their anti-inflammatory potencies, suggesting a common mechanism. (R,S)-ketorolac was significantly more potent than INDO or DS in vivo. Neither difference in relative potency of COX inhibition for (R,S)-ketorolac over INDO and DS nor activity of (S)-ketorolac at a number of other enzymes, channels, or receptors could account for the differences in observed potency. The distribution coefficient for (R,S)-ketorolac was approximately 30-fold less than for DS or INDO, indicating that (R,S)-ketorolac is much less lipophilic than these NSAIDs. Therefore, the physicochemical and pharmacokinetics properties of (R,S)-ketorolac may optimize the concentrations of (S)-ketorolac at its biological target(s), resulting in greater efficacy and potency in vivo.  (+info)

Inhibition of endothelium-dependent hyperpolarization by endothelial prostanoids in guinea-pig coronary artery. (4/3239)

1. In smooth muscle of the circumflex coronary artery of guinea-pig, acetylcholine (ACh, 10(-6) M) produced an endothelium-dependent hyperpolarization consisting of two components. An initial component that occurs in the presence of ACh and a slow component that developed after ACh had been withdrawn. Each component of the hyperpolarization was accompanied by an increase in membrane conductance. 2. Indomethacin (5 x 10(-6) M) or diclofenac (10(-6) M), both inhibitors of cyclooxygenase, abolished only the slow hyperpolarization. The initial hyperpolarization was not inhibited by diclofenac nor by nitroarginine, an inhibitor of nitric oxide synthase. 3. Both components of the ACh-induced hyperpolarization were abolished in the presence of atropine (10(-6) M) or high-K solution ([K+]0 = 29.4 mM). 4. The interval between ACh-stimulation required to generate an initial hyperpolarization of reproducible amplitude was 20 min or greater, but it was reduced to less than 5 min after inhibiting cyclooxygenase activity. Conditioning stimulation of the artery with substance P (10(-7) M) also caused a long duration (about 20 min) inhibition of the ACh-response. 5. The amplitude of the hyperpolarization generated by Y-26763, a K+-channel opener, was reproducible within 10 min after withdrawal of ACh. 6. Exogenously applied prostacyclin (PGI2) hyperpolarized the membrane and reduced membrane resistance in concentrations over 2.8 x 10(-9)M. 7. At concentrations below threshold for hyperpolarization and when no alteration of membrane resistance occurred, PGI2 inhibited the initial component of the ACh-induced hyperpolarization. 8. It is concluded that endothelial prostanoids, possibly PGI2, have an inhibitory action on the release of endothelium-derived hyperpolarizing factor.  (+info)

The cyclo-oxygenase-dependent regulation of rabbit vein contraction: evidence for a prostaglandin E2-mediated relaxation. (5/3239)

1. Arachidonic acid (0.01-1 microM) induced relaxation of precontracted rings of rabbit saphenous vein, which was counteracted by contraction at concentrations higher than 1 microM. Concentrations higher than 1 microM were required to induce dose-dependent contraction of vena cava and thoracic aorta from the same animals. 2. Pretreatment with a TP receptor antagonist (GR32191B or SQ29548, 3 microM) potentiated the relaxant effect in the saphenous vein, revealed a vasorelaxant component in the vena cava response and did not affect the response of the aorta. 3. Removal of the endothelium from the venous rings, caused a 10 fold rightward shift in the concentration-relaxation curves to arachidonic acid. Whether or not the endothelium was present, the arachidonic acid-induced relaxations were prevented by indomethacin (10 microM) pretreatment. 4. In the saphenous vein, PGE2 was respectively a 50 and 100 fold more potent relaxant prostaglandin than PGI2 and PGD2. Pretreatment with the EP4 receptor antagonist, AH23848B, shifted the concentration-relaxation curves of this tissue to arachidonic acid in a dose-dependent manner. 5. In the presence of 1 microM arachidonic acid, venous rings produced 8-10 fold more PGE2 than did aorta whereas 6keto-PGF1alpha and TXB2 productions remained comparable. 6. Intact rings of saphenous vein relaxed in response to A23187. Pretreatment with L-NAME (100 microM) or indomethacin (10 microM) reduced this response by 50% whereas concomitant pretreatment totally suppressed it. After endothelium removal, the remaining relaxing response to A23187 was prevented by indomethacin but not affected by L-NAME. 7. We conclude that stimulation of the cyclo-oxygenase pathway by arachidonic acid induced endothelium-dependent, PGE2/EP4 mediated relaxation of the rabbit saphenous vein. This process might participate in the A23187-induced relaxation of the saphenous vein and account for a relaxing component in the response of the vena cava to arachidonic acid. It was not observed in thoracic aorta because of the lack of a vasodilatory receptor and/or the poorer ability of this tissue than veins to produce PGE2.  (+info)

Nitric oxide limits the eicosanoid-dependent bronchoconstriction and hypotension induced by endothelin-1 in the guinea-pig. (6/3239)

1. This study attempts to investigate if endogenous nitric oxide (NO) can modulate the eicosanoid-releasing properties of intravenously administered endothelin-1 (ET-1) in the pulmonary and circulatory systems in the guinea-pig. 2. The nitric oxide synthase blocker N(omega)-nitro-L-arginine methyl ester (L-NAME; 300 microM; 30 min infusion) potentiated, in an L-arginine sensitive fashion, the release of thromboxane A2 (TxA2) stimulated by ET-1, the selective ET(B) receptor agonist IRL 1620 (Suc-[Glu9,Ala11,15]-ET-1(8-21)) or bradykinin (BK) (5, 50 and 50 nM, respectively, 3 min infusion) in guinea-pig isolated and perfused lungs. 3. In anaesthetized and ventilated guinea-pigs intravenous injection of ET-1 (0.1-1.0 nmol kg(-1)), IRL 1620 (0.2-1.6 nmol kg(-1)), BK (1.0-10.0 nmol kg(-1)) or U 46619 (0.2-5.7 nmol kg(-1)) each induced dose-dependent increases in pulmonary insufflation pressure (PIP). Pretreatment with L-NAME (5 mg kg(-1)) did not change basal PIP, but increased, in L-arginine sensitive manner, the magnitude of the PIP increases (in both amplitude and duration) triggered by each of the peptides (at 0.25, 0.4 and 1.0 nmol kg(-1), respectively), without modifying bronchoconstriction caused by U 46619 (0.57 nmol kg(-1)). 4. The increases in PIP induced by ET-1, IRL 1620 (0.25 and 0.4 nmol kg(-1), respectively) or U 46619 (0.57 nmol kg(-1)) were accompanied by rapid and transient increases of mean arterial blood pressure (MAP). Pretreatment with L-NAME (5 mg kg(-1); i.v. raised basal MAP persistently and, under this condition, subsequent administration of ET-1 or IRL 1620, but not of U-46619, induced hypotensive responses which were prevented by pretreatment with the cyclo-oxygenase inhibitor indomethacin. 5. Thus, endogenous NO appears to modulate ET-1-induced bronchoconstriction and pressor effects in the guinea-pig by limiting the peptide's ability to induce, possibly via ET(B) receptors, the release of TxA2 in the lungs and of vasodilatory prostanoids in the systemic circulation. Furthermore, it would seem that these eicosanoid-dependent actions of ET-1 in the pulmonary system and on systemic arterial resistance in this species are physiologically dissociated.  (+info)

Role of iNOS in the vasodilator responses induced by L-arginine in the middle cerebral artery from normotensive and hypertensive rats. (7/3239)

1. The substrate of nitric oxide synthase (NOS), L-arginine (L-Arg, 0.01 microM - 1 mM), induced endothelium-independent relaxations in segments of middle cerebral arteries (MCAs) from normotensive Wistar-Kyoto (WKY) and hypertensive rats (SHR) precontracted with prostaglandin F2alpha (PGF2alpha). These relaxations were higher in SHR than WKY arteries. 2. L-N(G)-nitroarginine methyl ester (L-NAME) and 2-amine-5,6-dihydro-6-methyl-4H-1,3-tiazine (AMT), unspecific and inducible NOS (iNOS) inhibitors, respectively, reduced those relaxations, specially in SHR. 3. Four- and seven-hours incubation with dexamethasone reduced the relaxations in MCAs from WKY and SHR, respectively. 4. Polymyxin B and calphostin C, protein kinase C (PKC) inhibitors, reduced the L-Arg-induced relaxation. 5. Lipopolysaccharide (LPS, 7 h incubation) unaltered and inhibited these relaxations in WKY and SHR segments, respectively. LPS antagonized the effect polymyxin B in WKY and potentiated L-Arg-induced relaxations in SHR in the presence of polymyxin B. 6. The contraction induced by PGF2alpha was greater in SHR than WKY arteries. This contraction was potentiated by dexamethasone and polymyxin B although the effect of polymyxin B was higher in SHR segments. LPS reduced that contraction and antagonized dexamethasone- and polymyxin B-induced potentiation, these effects being greater in arteries from SHR. 7. These results suggest that in MCAs: (1) the induction of iNOS participates in the L-Arg relaxation and modulates the contraction to PGF2alpha; (2) that induction is partially mediated by a PKC-dependent mechanism; and (3) the involvement of iNOS in such responses is greater in the hypertensive strain.  (+info)

Acute haemodynamic and proteinuric effects of prednisolone in patients with a nephrotic syndrome. (8/3239)

BACKGROUND: Administration of prednisolone causes an abrupt rise in proteinuria in patients with a nephrotic syndrome. METHODS: To clarify the mechanisms responsible for this increase in proteinuria we have performed a placebo controlled study in 26 patients with a nephrotic syndrome. Systemic and renal haemodynamics and urinary protein excretion were measured after prednisolone and after placebo. RESULTS: After i.v. administration of 125-150 mg prednisolone total proteinuria increased from 6.66+/-4.42 to 9.37+/-6.07 mg/min (P<0.001). By analysing the excretion of proteins with different charge and weight (albumin, transferrin, IgG, IgG4 and beta2-microglobulin) it became apparent that the increase of proteinuria was the result of a change in size selectivity rather than a change in glomerular charge selectivity or tubular protein reabsorption. Glomerular filtration rate rose from 83+/-34 ml to 95+/-43 ml/min (P<0.001) after 5 h, whereas effective renal plasma flow and endogenous creatinine clearance remained unchanged. As a result filtration fraction was increased, compatible with an increased glomerular pressure, which probably contributes to the size selectivity changes. Since corticosteroids affect both the renin-angiotensin system and renal prostaglandins, we have evaluated the effects of prednisolone on proteinuria after pretreatment with 3 months of the angiotensin-converting enzyme inhibitor lisinopril or after 2 weeks of the prostaglandin synthesis inhibitor indomethacin. Neither drug had any effect on prednisolone-induced increases of proteinuria. CONCLUSIONS: Prednisolone increases proteinuria by changing the size selective barrier of the glomerular capillary. Neither the renin-angiotensin axis nor prostaglandins seem to be involved in these effects of prednisolone on proteinuria.  (+info)

The effect of selective and non-selective cyclooxygenase inhibitors and nitric oxide on renal ischaemia-reperfusion injury in the normotensive and hypertensive rat ...
1. The effect of acetylsalicylic acid (ASA, 3 g/day for 3 days) and of indomethacin (IND, 150 mg/day for 3 days) on diuresis and on the excretion of prostaglandin E2 (PGE2) was studied in six healthy, male volunteers. After overnight deprivation the subjects received an oral water load (20 ml/kg) and hourly urine volumes were replaced by an equivalent volume of water by mouth for 4 h.. 2. Pretreatment with both ASA and IND induced a comparable suppression (P,0.05 to ,0.001) in the excretion of PGE2, but only IND also reduced (P,0.05) diuresis, free water clearance and the excretion of sodium. The excretion of creatinine was uninfluenced by both ASA and IND.. 3. These data indicate that a mechanism other than cyclo-oxygenase inhibition is involved in the effect of IND and ASA on diuresis in man. ...
TY - JOUR. T1 - Failure of cyclo-oxygenase inhibition to protect against arrhythmias induced by ischaemia and reperfusion. T2 - Implications for the role of prostaglandins as endogenous myocardial protective substances. AU - Wainwright, Cherry L.. AU - Parratt, J.. PY - 1991/1/1. Y1 - 1991/1/1. N2 - Study objective - It has been suggested that the balance between the release from the heart of prostacyclin and thromboxane A2 is a major determinant of the severity of arrhythmias during ischaemia and reperfusion. This has been examined in a dog model.Design - Three different cyclo-oxygenase inhibitors in doses adequate to prevent formation of both prostacyclin and thromboxane - aspirin (7 mg·kg-1), flurbiprofen (3 mg·kg-1), and sodium meclofanate (2 mg·kg-1) with or without nafazatrom or dazmegrel -were given prior to a combined occlusion-reperfusion insult, and the severity of resulting arrhythmias examined.Material - Adult greyhound dogs were used: controls n = 29; aspirin n = 10; flurbiprofen ...
The effects of selective ((5,5-dimethyl-3-(3-florophenyl)-4-(4-methylsulphonyl-2(5H)-furanon); DFU) and (N-(2-cyclohexyloxy-4-nitrophenyl)-methansulphonamide; NS 398)) or non-selective (diclophenac and proquazon) inducible cyclooxygenase (COX-2) inhibitors on the survival, nitrite (stable product of nitric oxide (NO) as an index for inducible NO synthase (iNOS) activity) and 6-keto-prostaglandin F-1alpha (6-keto-PGF(1alpha), stable product of prostacyclin as an index for COX-2 activity) production in serum, lungs, brain and/or kidney were investigated in endotoxin-induced sepsis model in mice. Endotoxin (10 mg kg(-1), i.p.)-induced mortality was prevented by DFU, NS 398 and proquazon (0.1, 10 and 1 mg kg(-1), respectively) and enhanced 2.6-fold with 0.1 mg kg(-1) diclophenac. Endotoxin-induced increase in the serum levels of nitrite was only inhibited by 10 mg kg(-1) diclophenac. Endotoxin caused a significant decrease only in the brain levels of nitrite without affecting 6-keto-PGF(1alpha) ...
Fingerprint Dive into the research topics of In vitro investigation of the interaction between nitric oxide and cyclo-oxygenase activity in equine ventral colon smooth muscle. Together they form a unique fingerprint. ...
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Etodolac (Lodine) is a COX inhibitor with an IC50 of 53.5 nM. Find all the information about Etodolac (Lodine) for cell signaling research.
Interleukin-1 (IL-1) induces hypophagia, which can be reduced by cyclooxygenase (COX) inhibitors. Earlier studies with COX knockout (COXko) mice suggested that COX2 was more important for hypophagia than COX1. However, behavioral responses occur long before COX2 is induced. Hypophagia was assessed in mice by measuring the intake of sweetened milk in a brief period. The intake was reduced within 30 min after intraperitoneal injection of IL-1β and was depressed for about 2 h. When milk intake was measured 30 to 40 min after IL-1β, COX1ko mice showed an attenuated response, whereas COX2ko mice responded more like wild-type animals. By contrast, 90 to 120 min after IL-1β COX1ko mice responded normally, whereas COX2ko mice showed only small responses. The COX2-selective inhibitor, celecoxib, failed to alter the response to IL-1β 30 min after administration, but low doses antagonized the effects of IL-1β at 90 to 120 min. The COX1-selective inhibitor, SC560, attenuated both the early and late ...
1. Overall mean pulmonary arterial pressure (MPAP)/cardiac index (CI) relationships were investigated in 13 pentobarbital anaesthetized dogs ventilated consecutively with a fraction of inspired O2 (F1o2) of 0.4 and with a F1o2 of 0.1. This sequence of alternated F1o2 0.4 and F1o2 0.1 was repeated (1) in the dogs with a strong pulmonary pressor response to hypoxia (more than 20% increase in pulmonary vascular resistance) (n = 6) under a continuous infusion of the leukotriene receptor blocker FPL 57231 (2 mg min−1 kg−1), and (2) in the dogs with a weak pressor response to hypoxia (n = 7) after cyclo-oxygenase inhibition by acetylsalicylic acid (1 g intravenously). Five-point MPAP/CI plots were constructed by opening a femoral arteriovenous fistula or by stepwise inflations of an inferior vena cava balloon catheter. The MPAP/CI plots were rectilinear in all experimental conditions.. 2. In responders, hypoxia was associated with an increase in MPAP over the entire range of CI studied (1-5 litres ...
BioAssay record AID 162654 submitted by ChEMBL: Inhibitory activity against human recombinant Prostaglandin G/H synthase 2 expressed in microsomes taken from baculovirus infected Sf9 cells.
Several studies suggest that cyclooxygenase-2 contributes to the delayed progression of ischemic brain damage. In this study we examined whether the highly selective cyclooxygenase-2 inhibitor DFU reduces neuronal damage when administered several hours after 5 min of transient forebrain ischemia in gerbils. The extent of ischemic injury was assessed behaviorally by measuring the increases in locomotor activity and by histopathological evaluation of the extent of CA1 hippocampal pyramidal cell injury 7 days after ischemia. DFU treatment (10 mg/kg, p.o.) significantly reduced hippocampal neuronal damage even if the treatment is delayed until 12 h after ischemia. These results suggest that selective cyclooxygenase-2 inhibitors may be a valuable therapeutic strategy for ischemic brain injury. ...
MAA699Hu22, PGG/HS; PGHS2; PHS2; HCox2; COX2; Cyclooxygenase 2; Prostaglandin G/H Synthase And Cyclooxygenase; Prostaglandin H2 synthase 2 | Products for research use only!
Because the levels of PGI synthase are comparable in the two muscle layers and do not vary with steroid treatments, it is tempting to conclude that the
Epidemiological and clinical studies suggest that non-steroidal anti-inflammatory drugs (NSAIDs), including cyclooxygenase (COX)-2 selective inhibitors, reduce the risk of developing cancer. Experimental studies in human cancer cell lines and rodent models of carcinogenesis support these observations by providing strong evidence for the antineoplastic properties of NSAIDs. The involvement of COX-2 in tumorigenesis and its overexpression in various cancer tissues suggest that inhibition of COX-2 is responsible for the chemopreventive efficacy of these agents. However, the precise mechanisms by which NSAIDs exert their antiproliferative effects are still a matter of debate. Numerous other studies have shown that NSAIDs can act through COX-independent mechanisms. This review provides a detailed description of the major COX-independent molecular targets of NSAIDs and discusses how these targets may be involved in their anticancer effects. Toxicities resulting from COX inhibition and the suppression of
Muller, M., Drew R., Heffernan, M., Blaha C., Sinoway, L. Penn State Hershey Heart and Vascular Institute, Penn State College of Medicine, Hershey, PA Prostaglandins are produced during skeletal muscle contraction and subsequently stimulate muscle afferent nerves, thereby contributing to the exercise pressor reflex (EPR). Humans with peripheral arterial disease (PAD) have an augmented EPR but the metabolite(s) responsible for this augmented response are not known. Purpose: We tested the hypothesis that intravenous infusion of ketorolac (a non-selective cyclooxygenase inhibitor that reduces prostaglandins) would attenuate the rise in mean arterial blood pressure (MAP) and heart rate (HR) in response to low-intensity plantar flexion exercise in humans with PAD. Methods: Six PAD patients underwent four minutes of one-legged rhythmic plantar flexion (30 contractions/min) in the supine posture. The workload began at 0.5 kg and progressed by 0.5 kg each minute. The leg with more severe PAD was always tested
Cyclooxygenase2 (COX-2), an inducible prostaglandin G/H synthase, is overexpressed in several human cancers. Here, the potential utility of selective COX-2 inhibitors in the prevention and treatment of cancer is considered. The mechanisms by which COX-2 levels increase in cancers, key data that indi …
Non steroidal drugs are mainly known for their activities and use as anti-inflammatory, antipyretic compounds. But, in recent observations, they are exposed to use as an effective alternative compounds to prevent or stimulate different metabolic activities and help in preventing various neoplastic progression. They have specific role in controlling estrogen metabolism during breast cancer progression. Sometimes, they are used as an apoptotic induction in various cancers. Their role in hypoxia induced proliferation is also showing promising results. Different NSAIDs will help to induce the activities of various tumor suppressor genes. As chronic inflammation increases the risk for various cancers, therefore, it is important to eliminate inflammation through anti-Inflammatory compounds where NSAIDs are playing a vital role. Most of them are acting to prevent inflammation either via selective or non-selective COX based mechanism. The non-selective COX inhibitor sulindac and the COX-2 selective ...
A simple explanation for this phenomenon would have been an upregulation of the ETA receptor expression. Surprisingly, immunofluorescent techniques and Western blot analysis revealed the opposite. Although the precise mechanism of ETA receptor-mediated downregulation remains to be established, there is evidence in the literature demonstrating that, eg, an upregulation of vascular endothelin-1 formed in an autocrine fashion may downregulate its own receptors.9. Increased constriction in response to ETA-receptor stimulation was markedly inhibited by the nonselective COX inhibitor indomethacin and by the TXA2/PGH2-receptor antagonist SQ-29548 pointing to a significant role of COX-derived prostanoids. Enhanced contraction to the ETA agonist was also substantially inhibited by celecoxib, a selective COX-2 inhibitor. Further evidence for a role of COX-2 was provided by Western blot analysis demonstrating that COX-2 expression was found to be increased in the media of eNOS knockout as compared with ...
A 740003 tumor development and angiogenesis had been first examined using sarcoma 180 cells that are allogeneic for ddy mice (Fig. 1) . In charge ddy mice treated with automobile solid tumors had been obvious 14 d after cell implantation. Daily oral administration of SC-560 the inhibitor functioning on COX-1 had simply no significant influence on tumor mass selectively. On the other hand the COX-2-selective inhibitors JTE-522 and NS-398 considerably decreased tumor mass as do aspirin a non-selective COX inhibitor (Fig. 1 A and D). The level of tumor-induced angiogenesis was evaluated based on hemoglobin items (Fig. 1 C) which correlated well using the vascular thickness in the tumor under histological evaluation (Fig. 1 B). In keeping with the proclaimed red color from the tumors angiogenesis was significant in vehicle-treated mice (Fig. 1 C and B. Like the results in tumor mass angiogenesis was significantly decreased by treatment with COX-2 inhibitors or aspirin however not with SC-560 (Fig. 1 ...
In this report, we present evidence that some NSAIDs increase the expression of an uncharacterized and divergent member of the TGF-β superfamily that we called NAG-1 (NSAIDs-activated gene). This protein possesses proapoptotic and antitumorigenic activity. Incubation of the cells with COX inhibitors at concentrations higher than required to inhibit COX initiated apoptosis and increased expression of NAG-1, suggesting a link between apoptosis and NAG-1 expression. Further evidence for this association between NAG-1 expression and apoptosis was obtained using NAG-1 sense and antisense transfected HCT-116 cells. Overexpression of NAG-1 in sense-NAG-1 cells enhanced basal and INDO-stimulated apoptosis, whereas the antisense-NAG-1 exhibited an attenuated response to INDO. Sense-NAG-1 HCT-116 colorectal cells display less clonogenic growth in soft agar than control HCT-116 cells. The reduction of colony growth in soft agar suggests that NAG-1 expression resulted in apoptosis and/or cell growth arrest ...
Disclosed is a pharmaceutical composition including a therapeutic quantity of a COX-2 inhibitor having an IC50-WHMA COX-2/COX-1 ratio ranging from about 0.23 to about 3.33 with reduced gastrointestinal and cardiovascular toxicity. Also disclosed are methods for treating osteoarthritis, rheumatoid arthritis or acute pain with less side-effects and faster onset of action utilizing the disclosed pharmaceutical composition.
Indomethacin | COX inhibitor | CAS [53-86-1] | Axon 3318 | Axon Ligand™ with >99% purity available from supplier Axon Medchem, prime source of life science reagents for your research
S-2474 is an inhibitor of COX-2 and 5-lipoxygenase (5-LO), with IC50s of 11 nM and 27 μM for COX-2 and COX-1 in human intact cells, and used as a nonsteroidal anti-inflammatory drug. - Mechanism of Action & Protocol.
two can be acting not solely via cAMP but additionally through PLC, which is usually a downstream effector of EP3 receptors (Asboth et al. 1996); PLC inhibition substantially decreased the response to PGE2 . PGE2 stimulates HA production in lots of other tissues too, such as atheroma (Marzoll et al. 2009). Moreover, synovium express the important synthetic enzymes COX1 and COX2 (Satoh et al. 2008). Nevertheless, PGE2 did not seem to mediate MSHA, since neither the common COX inhibitor indomethacin nor a combination ofC2009 The Authors. Journal compilationC2009 The Physiological SocietyJ Physiol 587.Pathways regulating movement-stimulated Altered functional expression of TRPV1168. To evaluate this possibility, we examined hyaluronan secretionspecific COX1 and COX2 inhibitors inhibited MSHA (Table four, study six). PGE2 In the mutants and also the genetically rescued worms in the WSA levels are raised in arthritis, where their pronounced HA-stimulating effect is probably to be vital in helping ...
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Indomethacin- ന്റെ ഉപയോഗങ്ങൾ, ഡോസേജ്, പാർശ്വഫലങ്ങൾ, പ്രയോജനങ്ങൾ, പ്രതിപ്രവർത്തനങ്ങൾ, മുന്നറിയിപ്പ് എന്നിവ കണ്ടെത്തുക
Background: Nonsteroidal anti-inflammatory drugs (NSAIDs) have been known to cause renal dysfunction in healthy patients and more pronounced renal effects in patients with cirrhosis and ascites. The use of NSAIDs have been associated with hepatorenal syndrome, a serious and often fatal complication associated with acute decline in renal function in the context of cirrhosis. However, renal safety of selective cyclo-oxygenase-2 (COX-2) and non-selective COX inhibitors has not been well delineated in current research with regards to patients with cirrhosis. This literature review seeks to compare the renal safety of selective and non-selective COX inhibitors in patients with cirrhosis. Methods: A thorough multi-database search was conducted using various combinations of keywords. Each study was evaluated using the Grading of Recommendations, Assessments, Development and Evaluation (GRADE) system. Results: Selective COX-2 inhibitor did not produce statistically significant decrements in renal function,
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Prostaglandin endoperoxide synthase 2, also referred to as cyclooxygenase 2 (COX-2), is a key enzyme in the conversion of arachidonic acid to prostaglandins and other eicosanoids. Rat intestinal epithelial (RIE) cells were permanently transfected with a COX-2 expression vector oriented in the sense …
Diclofenac Sodium - CAS 15307-79-6 - Calbiochem A cell-permeable, non-selective cyclooxygenase inhibitor (IC₅₀ = 60 nM and 200 nM for ovine COX-1 and COX-2 respectively) and potent non-steroidal anti-inflammatory drug with analgesic activity. - Find MSDS or SDS, a COA, data sheets and more information.
This study demonstrated dose-related excess mortality associated with the use of NSAIDs in patients with prior MI. There was a trend for increased risk of rehospitalization for MI, although the dose-related response in risk was not as clear as for death.. The VIGOR study was the first to report increased cardiovascular risk associated with the selective COX-2 inhibitors.1 Since then, several studies,5,6,8,12,23 although not all,2,24-26 have confirmed the findings. Several recently published observational studies have also indicated an increased cardiovascular risk associated with the nonselective NSAIDs.7-9,13. The present study is the first to address the risk of all NSAIDs in a selected population of post-MI patients. These patients are elderly, are frequently treated with NSAIDs, and have a high risk of additional cardiovascular events. Many of the randomized trials have excluded these patients. The results of the present study indicate acute or subacute effects of both the selective COX-2 ...
BACKGROUND: Adverse reactions to nonsteroidal antiinflammatory drugs (NSAIDs) are frequently reported, particularly among asthmatic patients. To date, there is no causal treatment available apart from tolerance induction. Therefore, the search for safe alternative drugs is of pivotal importance in clinical practice.. OBJECTIVE: The aim of our prospective study was to investigate the tolerance to celecoxib, a selective cyclooxygenase-2 inhibitor, in a large group of patients with positive case history of NSAID intolerance in comparison to paracetamol and nimesulide.. METHODS: 106 NSAID-sensitive patients, 46 (43.4%) of whom had experienced reactions only to one NSAID (single hypersensitivity), 60 (56.6%) to several NSAIDs (multiple hypersensitivity), were included in a single-blinded drug challenge protocol with cumulative doses of 175 mg of celecoxib, 875 mg of paracetamol and 175 mg of nimesulide. Objective and subjective symptoms during challenge were documented.. RESULTS: Of 261 challenges in ...
TY - GEN. T1 - Development of NSAIDs with lower gastric side effect. AU - Mizushima, Tohru. PY - 2012/6. Y1 - 2012/6. N2 - The anti-inflammatory action of nonsteroidal anti-inflammatory drugs (NSAIDs) is mediated through their inhibitory effects on cyclooxygenase (COX) activity. On the other hand, NSAIDs use is associated with gastrointestinal complications. The inhibition of COX by NSAIDs is not the sole explanation for the gastrointestinal side effects of NSAIDs. In this article, I review our recent work on the COX-independent mechanism involved in NSAID-induced gastric lesions. Using DNA microarray analysis, we found that NSAIDs affect expression of various genes in a COX-independent manner and found that membrane permeabilization activity of NSAIDs and resulting NSAID-induced apoptosis are involved in NSAID-induced gastric lesions. These results suggest that NSAIDs with lower membrane permeabilization activity would be safer on stomach tissue and we found that loxoprofen, a clinically used ...
This is the first study to demonstrate that a selective COX-2 inhibitor on top of standard therapy improves endothelial function and reduces markers of inflammation and oxidative stress in patients with coronary artery disease. Recognition that COX-2 is an inducible enzyme particularly associated with inflammation led to the development of selective COX-2 inhibitors that offer comparable efficacy and fewer unwanted side effects attributable to COX-1 inhibition, gastric ulceration in particular.1,2 Gastrointestinal safety of selective COX-2 inhibitors, however, may come at the cost of increased cardiovascular events, as suggested by the results of the VIGOR trial.5 Cardiovascular safety of coxibs was additionally challenged by studies in mice deficient in the PGI2 or TXA2 receptor.10 PGI2 receptor-deficient animals showed enhanced injury-induced vascular proliferation and platelet activation that was abolished in mice deficient of both PGI2 and TXA2 receptor, suggesting that PGI2 inhibition with ...
When we considered all the randomised trial data, selective COX 2 inhibitors were associated with a highly significant 1.4-fold increased risk of serious vascular events, largely due to a twofold increased risk of myocardial infarction. Although we found no significant excesses in the incidence of stroke or vascular death, the confidence intervals for each were wide, so we could not exclude a clinically important excess. If, as some people have suggested (on the basis of the delayed divergence of survival curves), the hazard emerges only after a year or 18 months,4 5 then combining short term and long term trials might underestimate the effects of long term exposure to a selective COX 2 inhibitor. We were not able to assess time dependent variation in the rate ratio because we sought numbers of events and person time only for the whole period of follow-up in each trial. However, as figure 2 clearly shows, when all the long term trials are considered, the summary rate ratio is similar to that ...
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Aspirin has three main therapeutic effects in the body: the antipyretic effect, the analgesic effect and the anti-inflammatory effect. This is due to the decreased production of prostaglandins and thromboxanes by the irreversible inactivation of the cyclooxygenase enzyme. Aspirin acts as an acetylating agent where an acetyl group is covalently attached to a serine residue in the active site of the COX enzyme[3]. This makes Aspirin different to other NSAIDS whereby they are reversible inhibitors and aspirin is not. The side effects are caused by the inhibition of COX-1 enzyme, which synthesises prostaglandin that serve essential physiological functions such as causing appropriate platelet aggregation, protection of the gastric mucosa, inhibition of thrombogenesis and maintenance of renal function. The therapeutic effects of NSAIDs are due to inhibition of COX-2, an enzyme induced by various factors released by bacteria, the vascular endothelium or other cells involved in the inflammatory ...
ptgs2, cox-2, cox2, gripghs, hcox-2, pgg/hs, pghs-2, phs-2; prostaglandin-endoperoxide synthase 2 (prostaglandin G/H synthase and cyclooxygenase); K11987 prostaglandin-endoperoxide synthase 2 [EC:] ...
Looking for online definition of Cyclo-oxygenase in the Medical Dictionary? Cyclo-oxygenase explanation free. What is Cyclo-oxygenase? Meaning of Cyclo-oxygenase medical term. What does Cyclo-oxygenase mean?
Patients with arthritis taking a COX-2 selective nonsteroidal anti-inflammatory drug (NSAID) appear to have a lower risk of adverse gastrointestinal events compared with those on a nonselective NSAID
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Intolerance of drug therapy often limits the usefulness of drugs that treat IBD. Adverse effects may be significant in some cases, thus requiring discontinuation of the therapy. Some of the nuances of IBD therapy are discussed below, focusing on the elderly, to encourage the tailoring of the medication regimen to the individual in conjunction with ongoing assessment (e.g., history and physical), close monitoring (e.g., selected laboratory tests), and evaluation of therapeutic outcomes. Avoiding NSAIDs: Reports have indicated that NSAIDs may trigger IBD occurrence or trigger exacerbation of underlying IBD; if possible, their use should be avoided.15,20,21 The mechanism by which this occurs is thought to be inhibition of prostaglandin production via cyclooxygenase inhibition that may impair mucosal barrier protection. If the benefit of treatment (e.g., of patients with symptomatic arthritis) outweighs the potential risk of IBD flare, the use of NSAIDs may be warranted in some patients.21 Of note, ...
Celecoxib and rofecoxib belong to a new class of NSAIDs that specifically inhibits COX-2. They have a significant anti-inflammatory and analgesic properties but are far less toxic than traditional NSAIDs, which inhibit both COX-1 and COX-2 (20 , 21) . However, not all COX-2 inhibitors share the same anticancer effects. The predictive discrepancy between the in vitro growth inhibitions of celecoxib and rofecoxib may be indicative of the difference in their mechanism of action. The present study provides the first direct comparison of the in vitro anticancer effects of the two clinically available COX-2 inhibitors.. The antiproliferative effect of celecoxib was noted to particularly inhibit the growth of the transformed but not the growth of the normal cells. Exposure to 10 μm celecoxib, for 72 h, inhibited transformed cell growth by 50% but had very little effect on the growth of normal cells (Fig. 1)⇓ . The IC50s of celecoxib ranges between 5 and 20 μm across this entire panel of cell lines. ...
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COX1 / Cyclooxygenase 1兔单克隆抗体[EPR5866](ab109025)可与小鼠, 大鼠, 人样本反应并经WB, IP, IHC, Flow Cyt, ICC/IF实验严格验证,被2篇文献引用并得到2个独立的用户反馈。
Cyclooxygenase is an enzyme that produces signals that can lead to pain and inflammation. Medications that inhibit cyclooxygenase...
Experts discuss the use of firocoxib in horses, including benefits of selective COX-2 inhibition, FDA restrictions, and the importance of proper dosing.
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Arti kata dari indomethacin. Definisi dari indomethacin. Pengertian dari indomethacin: a nonsteroidal anti-inflammatory drug (trade name Indocin);
Celecoxib belongs to the group of medications called selective COX-2 inhibitors, which is a kind of nonsteroidal anti-inflammatory drugs (NSAIDs). NSAIDs work by reducing a substance in the body that leads to inflammation (swelling) and pain.
Celecoxib belongs to the group of medications called selective COX-2 inhibitors, which is a kind of nonsteroidal anti-inflammatory drugs (NSAIDs). NSAIDs work by reducing a substance in the body that leads to inflammation (swelling) and pain.
Priva-Celecoxib: Celecoxib belongs to the group of medications called selective COX-2 inhibitors, which is a kind of nonsteroidal anti-inflammatory drugs (NSAIDs). NSAIDs work by reducing a substance in the body that leads to inflammation (swelling) and pain.
Riva-Celecoxib: Celecoxib belongs to the group of medications called selective COX-2 inhibitors, which is a kind of nonsteroidal anti-inflammatory drugs (NSAIDs). NSAIDs work by reducing a substance in the body that leads to inflammation (swelling) and pain.
Professor Mitchell added: This review shows us that despite the large scale use of NSAIDs and COX-2 inhibitors for a number of years, we still need more information on their benefits and potential risks and that more research needs to be done in this area. Looking at existing evidence, however, it would seem COX-2 inhibitors may be the best option for some patients. They are as effective as traditional NSAIDs, but with less gastric side effects than some older drugs ...
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Any medical peeps about? Due to a medical issue Ive been prescribed very strong dose naproxen more than I usually take. For internal swelling (try
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ab120295 NS 398, COX-2 inhibitor (CAS番号: 123653-11-2) 分子量: 314.36 化学式: C13H18N2O5S COX-2 阻害剤 アブカムの高純度な生理活性物質(アゴニスト・アンタゴニスト・アクティベーター・阻害剤)
Интерлеукин 17A је протеин који је код људи кодиран IL17A геном.[1][2][3] Протеин кодиран овим геном је проинфламаторни цитокин произведен активираним Т ћелијама.[4] Овај цитокин регулише активности НФ-капаБ и митоген активираних протеин киназа. Овај цитокин може да стимулише изражавање ИЛ-6 и циклооксигеназе-2 (PTGS2/COX-2), као и да појача продукцију нитрик оксида (NO). Високи нивои овог цитокина су асоцирани са неколико хроничних инфламаторних обољења укључујући реуматоидни артритис, псоријазу и мултиплу склерозу.[2] ...
FitzGerald, Garret (2001). "COX-2 inhibitors and the cardiovascular system". Clin Exp Rheumatol. 19 (6 Suppl 25): S31-6. PMID ...
Peres MF, Silberstein SD (2002). "Hemicrania continua responds to cyclooxygenase-2 inhibitors". Headache. 42 (6): 530-1. doi: ...
A highly selective reversible inhibitor of the COX-2 isoform of cyclooxygenase, celecoxib inhibits the transformation of ... Nonselective NSAIDs (such as aspirin, naproxen, and ibuprofen) inhibit both COX-1 and COX-2. Inhibition of COX-1 (which ... The COX-2 inhibitor rofecoxib (Vioxx) was removed from the market in 2004 due to its risk. Like all NSAIDs on the US market, ... which is an isoleucine in COX-1 and a valine in COX-2. This mutation appears to contribute to COX-2 selectivity by creating ...
"Cannabinoid system and cyclooxygenases inhibitors". Journal of Medicine and Life. 4 (1): 11-20. PMC 3056416. PMID 21505570. ... or cyclooxygenase (COX), to produce ethanolamide oxylipins, like prostaglandin ethanolamides (prostamide) by COX-2, with ... The major COX-2 derived prostanoid product from NAE 20:4 (AEA) are prostaglandin E2 (PGE2) ethanolamide (PGE2-EA; prostamide E2 ... FAAH inhibitors are seen to both increase alcohol consumption (NAE 20:4; AEA) and prevent against oxidative stress caused by ...
COX-1 by aspirin apparently results in the upregulation of COX-2 as part of a gastric defense and that taking COX-2 inhibitors ... COX-1 and COX-2, are acted on by aspirin. Aspirin irreversibly inhibits COX-1 and modifies the enzymatic activity of COX-2. COX ... Warner TD, Mitchell JA (October 2002). "Cyclooxygenase-3 (COX-3): filling in the gaps toward a COX continuum?". Proceedings of ... However, several COX-2 inhibitors, such as rofecoxib (Vioxx), have been withdrawn from the market, after evidence emerged that ...
Both COX-2 inhibitors and other non-selective NSAIDS have potential adverse effects that include damage to the kidneys. These ... as well as the IL-12/IL-23 inhibitor ustekinumab, and the IL-17a inhibitor secukinumab. Recently, the Jak inhibitor, ... Coxibs (COX-2 inhibitors) e.g. Celecoxib or Etoricoxib, are associated with a statistically significant 50 to 66% relative risk ... Kearney PM, Baigent C, Godwin J, Halls H, Emberson JR, Patrono C (Jun 2006). "Do selective cyclo-oxygenase-2 inhibitors and ...
... a COX-2 inhibitor; and LY311727, an inhibitor of secretory phospholipase. Currently, one of the most interesting applications ...
Hawkey CJ (October 2001). "COX-1 and COX-2 inhibitors". Best Practice & Research. Clinical Gastroenterology. 15 (5): 801-20. ... "Effect of COX-1/COX-2 inhibition versus selective COX-2 inhibition on coronary vasodilator responses to arachidonic acid and ... Naproxen is a nonselective COX inhibitor. It is in the propionic acid class of medications. As an NSAID, naproxen appears to ... Rodrigues AD (November 2005). "Impact of CYP2C9 genotype on pharmacokinetics: are all cyclooxygenase inhibitors the same?". ...
Sharma, S.; Sharma, S. C. (1997). "An update on eicosanoids and inhibitors of cyclooxygenase enzyme systems". Indian Journal of ... Tóth, L.; Muszbek, L.; Komaromi, I. (2013). "Mechanism of the irreversible inhibition of human cyclooxygenase-1 by aspirin as ... The mechanism of action of aspirin involves irreversible inhibition of the enzyme cyclooxygenase; therefore suppressing the ... aspirin is the only NSAID that irreversibly inhibits COX-1. Some drug mechanisms of action are still unknown. However, even ...
Aspirin and other cyclooxygenase inhibitors can significantly prolong bleeding time. While warfarin and heparin have their ...
Most oxicams are unselective inhibitors of the cyclooxygenase (COX) enzymes. The exception is meloxicam with a slight (10:1) ... preference for COX-2, which, however, is only clinically relevant at low doses. Examples include: Ampiroxicam Piroxicam ...
However, several COX-2 selective inhibitors have subsequently been withdrawn after evidence emerged that COX-2 inhibitors ... Newer NSAID drugs called COX-2 selective inhibitors have been developed that inhibit only COX-2, with the hope for reduction of ... Warner, T. D; Mitchell, J. A (2002). "Cyclooxygenase-3 (COX-3): Filling in the gaps toward a COX continuum?". Proceedings of ... There are at least two different cyclooxygenase isozymes: COX-1 (PTGS1) and COX-2 (PTGS2). Aspirin is non-selective and ...
Zhang J, Ding EL, Song Y (October 2006). "Adverse effects of cyclooxygenase 2 inhibitors on renal and arrhythmia events: meta- ... It is a selective cyclooxygenase-2 inhibitor. It was patented in 1995. Valdecoxib was manufactured and marketed under the brand ... Discovery and development of cyclooxygenase 2 inhibitors Parecoxib Apricoxib Fischer J, Ganellin CR (2006). Analogue-based Drug ... Alert on Bextra withdrawal Large systematic review of adverse renal and arrhythmia risk of valdcoxib and other COX-2 inhibitors ...
... is a platelet aggregation inhibitor. It acts as a reversible cyclooxygenase inhibitor. The Merck Index (12th ed.). p ...
It acts as a COX-2 inhibitor. Mavacoxib, along with other COX-2 selective inhibitors, celecoxib, valdecoxib, and parecoxib, ... October 2010). "The pharmacokinetics of mavacoxib, a long-acting COX-2 inhibitor, in young adult laboratory dogs". Journal of ... European Public Assessment Report (EPAR): Trocoxil, European Medicines Agency Cox SR, Lesman SP, Boucher JF, Krautmann MJ, ...
It acts as a COX-2 inhibitor. Reaction of the imine with TosMIC in the presence of potassium carbonate leads to what may be ... Activity Relationship of a New Series of COX-2 Selective Inhibitors: 1,5-Diarylimidazoles". Journal of Medicinal Chemistry. 46 ...
It is a COX-2 inhibitor (coxib). Gaynor JS, Muir WM (2014). "Robenacoxib". Handbook of Veterinary Pain Management (3rd, revised ...
... the COX-2 inhibitors Celebrex and Bextra; Ambien for insomnia; and NutraSweet (also known as aspartame), an artificial ... which Searle developed and which became the first selective COX-2 inhibitor to be approved by the FDA on December 31, 1998. ...
COX-2 inhibitors[edit]. Main article: COX-2 inhibitor. These drugs have been derived from NSAIDs. The cyclooxygenase enzyme ... Reversible COX-1/COX-2 inhibitor.. Ophthalmologic.. N/A. Postoperative pain and inflammation.. Corneal ulceration. ... Reversible COX-1/COX-2 inhibitor.. PO and topical.. Bioavailability = 50-60%; protein binding = 99-99.8%; hepatic metabolism; ... COX-2 selective inhibitors Celecoxib. Comes in free form; practically insoluble in water, fairly soluble in organic solvents. ...
Aspirin and other NSAIDs are inhibitors of the cyclooxygenases. In the kidney, this inhibition results in decreased PGE2 ... Inhibition of cyclooxygenases therefore rather selectively damages the renal papillae, increasing the risk of renal papillary ... In cells of the kidney, cyclooxygenases catalyse the conversion of paracetamol into N-acetyl-p-benzoquinoneimine (NAPQI). NAPQI ... Like all prostaglandins, PGE2 synthesis depends upon the cyclooxygenases.[citation needed] ...
Most NSAIDs act as nonselective inhibitors of the cyclooxygenase (COX) enzymes, inhibiting both the cyclooxygenase-1 (COX-1) ... and it is inhibition of COX-2 that produces the desirable effects of NSAIDs. When nonselective COX-1/COX-2 inhibitors (such as ... Non-steroidal anti-inflammatory drugs (NSAIDs) are the competitive inhibitors of cyclooxygenase (COX), the enzyme which ... NSAIDs work by inhibiting the activity of cyclooxygenase enzymes (COX-1 or COX-2). In cells, these enzymes are involved in the ...
Day, Richard O.; Graham, Garry G. (1 December 2004). "The Vascular Effects of COX-2 selective inhibitors". Australian ... NSAIDs such as Ibuprofen/paracetamol work to reduce the immediate inflammation by inhibiting Cox-1 and Cox-2 enzymes, which are ...
COX-1, such as the COX-2 inhibitors celecoxib and rofecoxib, also are regarded as safe. Nonetheless, recent studies do find ... caution is recommended in using any COX inhibitors. In addition to aspirin and NSAIDs, consumption of even small amounts of ... and to any medication that inhibits the cyclooxygenase-1 (COX-1) enzyme, although paracetamol (acetaminophen) in low doses is ... Leukotriene antagonists and inhibitors (montelukast, zafirlukast, and zileuton) often are helpful in treating the symptoms of ...
... it binds to a different site on the COX-2 enzyme than do other COX-2 inhibitors; it is the only acidic coxib and has the ... Lumiracoxib is a COX-2 selective inhibitor nonsteroidal anti-inflammatory drug. Its structure is different from that of other ... Shi, S; Klotz, U (March 2008). "Clinical use and pharmacological properties of selective COX-2 inhibitors". European Journal of ... Tacconelli S, Capone ML, Patrignani P (2004). "Clinical pharmacology of novel selective COX-2 inhibitors". Curr Pharm Des. 10 ( ...
Traditional NSAIDs and COX-2 inhibitor NSAIDs are effective for treating axSpA. The potential harms may not differ when ...
Immunosuppressant drugs such as corticosteroids, cyclooxygenase inhibitors, interferon alpha may be effective. In June 2018 NHS ...
March 2004). "The cyclooxygenase isozyme inhibitors parecoxib and paracetamol reduce central hyperalgesia in humans". Pain. 108 ...
No COX-2 selective inhibitor has been approved in the US since that time, regardless of the safety profile of parecoxib in ... Gajraj NM (2007). "COX-2 inhibitors celecoxib and parecoxib: valuable options for postoperative pain management". Current ... Parecoxib is the first parenteral COX-2 selective inhibitor available for clinical use in pain management. It is well known ... Parecoxib, along with other COX-2 selective inhibitors, celecoxib, valdecoxib, and mavacoxib, were discovered by a team at the ...
COX-2 selective inhibitor Discovery and development of cyclooxygenase 2 inhibitors David Graham (epidemiologist) "Vioxx PI" ( ... Cyclooxygenase (COX) has two well-studied isoforms, called COX-1 and COX-2. COX-1 mediates the synthesis of prostaglandins ... Rofecoxib is a selective COX-2 inhibitor, or "coxib". Though the class of coxibs includes several agents, there are varying ... Zhang J, Ding EL, Song Y (October 2006). "Adverse effects of cyclooxygenase 2 inhibitors on renal and arrhythmia events: meta- ...
Phenethyl ferulate, which is a cyclooxygenase inhibitor in vitro. Notopterygium incisum. Flora of China. Retrieved June 20, ... Zschocke, S; Lehner, M; Bauer, R (1997). "5-Lipoxygenase and cyclooxygenase inhibitory active constituents from Qianghuo ( ...
Yi, John S.; Cox, Maureen A.; Zajac, Allan J. T-cell exhaustion: characteristics, causes and conversion. Immunology. 2010-04, ... U.S. FDA Approved Immune-Checkpoint Inhibitors and Immunotherapies. Medical Writer Agency , 香港醫學作家 , MediPR , MediPaper Hong ...
... the high risk of birth defects with 5α-reductase inhibitors limits their use in women.[1][138] However, 5α-reductase inhibitors ... Simpson NB, Cunliffe WJ (2004). "Disorders of the sebaceous glands". In Burns, Tony, Breathnach, Stephen, Cox, Neil, Griffiths ... Azzouni F, Zeitouni N, Mohler J (February 2013). "Role of 5α-reductase inhibitors in androgen-stimulated skin disorders". ... and inhibitors of the stearoyl-CoA desaturase-1 enzyme are also a focus of research efforts.[10][91] Particles that release ...
March 2004). "The cyclooxygenase isozyme inhibitors parecoxib and paracetamol reduce central hyperalgesia in humans". Pain. 108 ...
5α-Reductase inhibitorsEdit. 5α-Reductase inhibitors such as finasteride and dutasteride are inhibitors of 5α-reductase, an ... Boris, A.; Scott, J. W.; DeMartino, L.; Cox, D. C. (1973). "ENDOCRINE PROFILE OF A NONSTEROIDAL ANTIANDROGEN N-(3,5-DIMETHYL-4- ... Androgen synthesis inhibitorsEdit. Androgen synthesis inhibitors are enzyme inhibitors that prevent the biosynthesis of ... androgen synthesis inhibitors can be further divided mostly into CYP17A1 inhibitors and 5α-reductase inhibitors; and ...
c-Met inhibitors. *Cyclooxygenase 2 inhibitors. *Dipeptidyl peptidase-4 inhibitors. *Direct thrombin inhibitors ...
is modified to include binding of the inhibitor to the free enzyme:. EI. +. S. ⇌. k. 3. k. −. 3. E. +. S. +. I. ⇌. k. −. 1. k. ... is the inhibitor concentration.. V. max. {\displaystyle V_{\max }}. remains the same because the presence of the inhibitor can ... To compute the concentration of competitive inhibitor [. I. ]. {\displaystyle {\ce {[I]}}}. that yields a fraction f. V. 0. {\ ... At this point, we can define the dissociation constant for the inhibitor as K. i. =. k. −. 3. /. k. 3. {\displaystyle K_{i}=k ...
Cox, PA; Banack, SA; Murch, SJ; Rasmussen, U; Tien, G; Bidigare, RR; Metcalf, JS; Morrison, LF; Codd, GA; Bergman, B. (2005). " ... UV protectants and specific inhibitors of enzymes.[16][17] ... Cox PA, Davis DA, Mash DC, Metcalf JS, Banack SA (2015). " ...
COX-2) pa je inducibilni encim, vključen v procese vnetja. Zaviranje COX-2 je odgovorno za terapevtske učinke, zaviranje COX-1 ... Thomas, Mc (februar 2000). "Diuretics, ACE inhibitors and NSAIDs-the triple whammy". The Medical journal of Australia. 172 (4 ... Sklepajo, da je COX-3 možno mesto delovanja paracetamola, vendar tudi drugi analgetiki in antipiretiki v in vitro poskusih ... Zaviranje COX 1 zato povzroča neželene učinke na prebavilih. Neželeni učinki na prebavila so močneje izraženi pri tistih NSAID ...
t-PA and urokinase are themselves inhibited by plasminogen activator inhibitor-1 and plasminogen activator inhibitor-2 (PAI-1 ... Factor Xa inhibitors. (with some II inhibition). Heparin group/. glycosaminoglycans/. (bind antithrombin). *Low molecular ... Coagulation inhibitors. *Antithrombin (inhibits II, IX, X, XI, XII). *Protein C (inhibits V, VIII)/Protein S (cofactor for ... Antifibrinolytics, such as aminocaproic acid (ε-aminocaproic acid) and tranexamic acid are used as inhibitors of fibrinolysis. ...
Inhibitors of squalene epoxidase have found application mainly as antifungal drugs: butenafine naftifine terbinafine Since ... Cox T, Jackson D, Severin J, Biggs P, Fu J, Nefedov M, de Jong PJ, Stewart AF, Bradley A (Jun 2011). "A conditional knockout ... "Transcriptional regulation of squalene epoxidase by sterols and inhibitors in HeLa cells". The Journal of Biological Chemistry ... squalene epoxidase is on the biosynthetic pathway leading to cholesterol, inhibitors of this enzyme may also find application ...
Simpson CR, Hippisley-Cox J, Sheikh A (July 2010). "Trends in the epidemiology of chronic obstructive pulmonary disease in ... and breakdown of the connective tissue of the lungs by proteases that are insufficiently inhibited by protease inhibitors. The ... are phosphodiesterase-4 inhibitors (PDE4) and act as anti-inflammatories. They show promise in decreasing the rate of ... "Phosphodiesterase-4 inhibitors for chronic obstructive pulmonary disease". The Cochrane Database of Systematic Reviews. 5 ...
The influence of isotretinoin and 5-a reductase inhibitors in metaloproteases of connective tissue in patients with ance] (in ... Goodfield MJ, Cox NH, Bowser A, McMillan JC, Millard LG, Simpson NB, Ormerod AD (June 2010). "Advice on the safe introduction ... the tissue inhibitors of metalloproteases).[69] It is already known that metalloproteases play an important role in the ...
COX-inhibiting nitric oxide donator: Naproxcinod. N-Arylanthranilic acids. (fenamates). *Azapropazone. *Clonixin ...
Sanger, F; Nicklen, S; Coulson, AR (1977). "DNA sequencing with chain-terminating inhibitors". Proceedings of the National ... Cox DR, James MR, Bentley D, Deloukas P, Lander ES, Hudson TJ (October 1996). "A gene map of the human genome". Science 274 ( ...
COX-2 inhibitors. *Celecoxib. *Etoricoxib. *Lumiracoxib. *Parecoxib. *Rofecoxib ‡. *Valdecoxib ‡. Fenamates. *Meclofenamic acid ...
COX-1)과 사이클로옥시제네이스-2(COX-2)를 저해하는 아스피린이 있다.[81] 다른 효소 저해제들 중에는 독으로 작용하는 것도 있다. 예를 들어, 사이안화물 독은 사이토크롬 c 산화효소의 활성 부위에 있는 구리 및 철과 ... Wlodawer A, Vondrasek J (1998). "Inhibitors of HIV-1 protease: a major success of structure-assisted drug design". 》Annual ... 가 나 다 라 마 David L. Nelson, Michael M. Cox. , 《Lehninger principles of biochemistry 4th》, New York : W. H. Freeman, 2005, 23~24 ... 가 나 다 라 마 David L. Nelson, Michael M. Cox. , 《Lehninger principles of biochemistry 4th》, New York : W. H. Freeman, 2005, 195~ ...
Cox M, Lehninger AL, Nelson DR (2000). Lehninger principles of biochemistry. New York: Worth Publishers. pp. 306-308. ISBN 1- ...
... is a weak inhibitor of dihydrofolate reductase,[69] but whether this effect is sufficient to contribute to a ... It is known that lamotrigine is a weak inhibitor of human dihydrofolate reductase (DHFR) and other, more powerful, human DHFR ... inhibitors like methotrexate are known to be teratogenic.[47] Lamotrigine is expressed in breast milk; the manufacturer does ...
HDAC inhibitor (small molecule) benzamide M344 MC 19 fatty acid Sodium butyrate M (y) 5, 6, 7 ; H (ny) D (y) 11 M (y) 14; R (y ... COX-2. At the individual gene level, hypomethylation and thus derepression of COX-2 occurs, inhibition of which reduces ... DNA methyltransferase inhibitors, and histone demethylase inhibitors.[6][7] The majority of epigenetic drugs tested for use ... DNA-methylation inhibitor chemical analogue of cytidine Azathioprine M (ny) M (ny) ...
Neuraminidase inhibitors. Overall the benefits of neuraminidase inhibitors in those who are otherwise healthy do not appear to ... Cox NJ, Subbarao K (October 1999). "Influenza". Lancet. 354 (9186): 1277-82. doi:10.1016/S0140-6736(99)01241-6. PMID 10520648. ... M2 inhibitors. The antiviral drugs amantadine and rimantadine inhibit a viral ion channel (M2 protein), thus inhibiting ... Bright RA, Medina MJ, Xu X, Perez-Oronoz G, Wallis TR, Davis XM, Povinelli L, Cox NJ, Klimov AI (October 2005). "Incidence of ...
The main categories of drugs for musculoskeletal disorders are: NSAIDs (including COX-2 selective inhibitors), muscle relaxants ... Anti-allergy: mast cell inhibitors. *Anti-glaucoma: adrenergic agonists, beta-blockers, carbonic anhydrase inhibitors/ ... HMG-CoA reductase inhibitors (statins) for lowering LDL cholesterol inhibitors: hypolipidaemic agents. ... cytotoxic drugs, therapeutic antibodies, sex hormones, aromatase inhibitors, somatostatin inhibitors, recombinant interleukins ...
"Matrix metalloproteinase inhibitors". Georgetown University Hospital, Vincent T. Lombardi Cancer Center, Division of Medical ... Selain itu, akan tampak ekspresi gen iNOS di sel vaskular maupun sel yang mengalami peradangan dan ekspresi gen COX-2 di sel ... "Reducing bleeding complications after thrombolytic therapy for stroke: clinical potential of metalloproteinase inhibitors and ... faktor jaringan dan tissue factor pathway inhibitor.[22] Disfungsi endotelial yang menyebabkan defisiensi sawar darah otak, ...
inhibitors). COX. (PTGS). *Salicylic acids: Aloxiprin. *Aspirin (acetylsalicylic acid). *Benorilate (benorylate). *Carbasalate ... In Europe, use of selexipag together with strong inhibitors of the liver enzyme [CYP2C8], such as gemfibrozil, is ...
Nelson, D. L.; Cox M. M. (2004). Lehninger Principles of Biochemistry (4th ed.). W. H. Freeman. ISBN 0-7167-4339-6.. ... Vigabatrin is an irreversible inhibitor of GABA transaminases which leads to decreased levels of GHB and elevation of GABA. ...
Cox BS (1965). "[PSI], a cytoplasmic suppressor of super-suppression in yeast". Heredity. 20 (4): 505-521. doi:10.1038/hdy. ... "The histone methyltransferase inhibitor BIX01294 enhances the cardiac potential of bone marrow cells.". Stem Cells Dev. 22: ... also shown a potential to differentiate into cardiac competent cells when treated with G9a histone methyltransferase inhibitor ...
... selective monoamine oxidase inhibitor,[5][6][9] and as a low affinity, non-competitive NMDA receptor antagonist.[1][2][10] A ... Mattia C, Coluzzi F (September 2007). "Indantadol, a novel NMDA antagonist and nonselective MAO inhibitor for the potential ... a N-methyl-D-aspartate receptor antagonist and monoamine oxidase-A inhibitor, attenuates secondary hyperalgesia in a human pain ... Monoamine reuptake inhibitors • Monoamine releasing agents • Monoamine neurotoxins ...
... shepherding the subunits of COX together into a functional protein complex. This results in a deficit of COX protein, reducing ... Murphy, Jerome V (1974). "Leigh Disease: Biochemical Characteristics of the Inhibitor". Archives of Neurology. 31 (4): 220-7. ... Mutations in mitochondrial DNA (mtDNA) and over 30 genes in nuclear DNA (gene SURF1[8] and some COX assembly factors) have been ... Kidney and heart tissues were found to not have a COX deficiency.[12] ...
Factor Xa inhibitors. (with some II inhibition). Heparin group/. glycosaminoglycans/. (bind antithrombin). *Low molecular ... Endogenous plasma protease inhibitors deactivate drotrecogin. Therefore, no dose adjustment is needed in elderly patients, or ... Recent administration (within 7 days) of ,650 mg/day of aspirin or other platelet inhibitors ... Recent administration (within 7 days) of oral anticoagulants or GP IIb/IIIa inhibitors ...
Lee IO, Seo Y (March 2008). "The effects of intrathecal cyclooxygenase-1, cyclooxygenase-2, or nonselective inhibitors on pain ... COX). Ketorolac is a non-selective COX inhibitor.[24] It is considered a first-generation NSAID.[20] ... Ketorolac works by blocking cyclooxygenase 1 and 2 (COX1 and COX2), thereby decreasing production of prostaglandins.[2][4] ... and analgesic effects is the inhibition of prostaglandin synthesis by competitive blocking of the enzyme cyclooxygenase ( ...
Nonsteroidal anti-inflammatory drug − cyclooxygenase inhibitor. *Proton-pump inhibitor. *Renin inhibitor. *Selective ... Enzyme target mechanisms include activator or inhibitor. Ion channel modulators include opener or blocker. The following are ...
... of NSAID expenditures were for COX-2 inhibitors. Over the period of the study, COX-2 inhibitors rose from 10.03% of total ... COX-2 appears to be related to cancers and abnormal growths in the intestinal tract. COX inhibitors have been shown to reduce ... Selective COX-2 inhibitors are a type of nonsteroidal anti-inflammatory drug (NSAID) that directly targets cyclooxygenase-2, ... The inhibition of COX-2 is paramount for the anti-inflammatory and analgesic function of the selective COX-2 inhibitor ...
COX-2 inhibitors are a type of nonsteroidal anti-inflammatory drug (NSAID) that directly targets cyclooxygenase-2, COX-2, an ... COX-2 inhibitors are currently being studied in breast cancer and appear to be beneficial. COX-2 inhibitors have been found to ... of NSAID expenditures were for COX-2 inhibitors. Over the period of the study, COX-2 inhibitors rose from 10.03% of total ... COX-2 appears to be related to cancers and abnormal growths in the intestinal tract. COX inhibitors have been shown to reduce ...
Cyclooxygenases have two main isoforms that are called COX-1 and COX-2 (as well as a COX-3). COX-1 is responsible for the ... Studies on the binding mechanism of selective COX-2 inhibitors show that they have two reversible steps with both COX-1 and COX ... Dup-697 became the building-block for synthesis of COX-2 inhibitors. Celecoxib and rofecoxib, the first COX-2 inhibitors to ... The bulky sulfonamide group in COX-2 inhibitors such as celecoxib and rofecoxib prevent the molecule from entering the COX-1 ...
... Laurel J. Mengle-Gaw and Benjamin D. Schwartz ... Laurel J. Mengle-Gaw and Benjamin D. Schwartz, "Cyclooxygenase-2 inhibitors: promise or peril?," Mediators of Inflammation, vol ...
However, the chief investigator is stressing that the study is not a reason for people to stop taking COX-2 inhibitors and that ... A new study in mice could help shed light on why COX-2 inhibitors might increase the risk of thrombotic events. ... "Rofecoxib is by far the most selective COX-2 inhibitor, with 70-100 times more selectivity for COX-2 over COX-1 compared with ... Philadelphia, PA - A new study in mice could help shed light on why COX-2 inhibitors might increase the risk of thrombotic ...
Cox 2 Inhibitor News and Research. RSS Cox-2 Inhibitors are nonsteroidal anti-inflammatory drugs used to relieve pain and ... COX-2 inhibitors are being studied in the prevention of colon polyps, and as anticancer drugs. Also called cyclo-oxygenase-2 ... By combining a COX-2 inhibitor, similar to Celebrex, and an epoxide hydrolase (sEH) inhibitor, the drug controls angiogenesis ( ... or cyclooxygenase-2 (COX-2) inhibitors, both of which can irritate the digestive tract. At times additional drugs are co- ...
Another COX-2 inhibitor has been shot down by the FDA. Having spent the last two months reviewing the safety of the COX-2- ... Rofecoxib is one of the new breed of anti-inflammatories known as COX-2 (cyclo-oxygenase-2) inhibitors that are supposed to be ... It employs a pioneering technology called COX-2 (selective cyclo oygenase 2 inhibitors), which is supposed to o ... ... But NSAIDs quickly became COX-2 inhibitors associated with adverse gastrointestinal effects such as peptic... ...
Cyclooxygenase 1 Inhibitor, Cyclooxygenase 2 Inhibitors, Cyclooxygenase Inhibitors, NF-kappaB Inhibitor, Proteasome Inhibitors ... Cyclooxygenase 1 Inhibitor, Cyclooxygenase 2 Inhibitors, Cyclooxygenase Inhibitors, NF-kappaB Inhibitor, Tumor Necrosis Factor ... Pharmacological Actions : Cyclooxygenase 1 Inhibitor, Cyclooxygenase 2 Inhibitors, Cyclooxygenase Inhibitors, Postaglandin PGE2 ... Cyclooxygenase 1 Inhibitor, Cyclooxygenase 2 Inhibitors, Cyclooxygenase Inhibitors, Prostaglandin PGE2 downregulation ...
Cyclooxygenase 1 Inhibitor : CK(34) : AC(27), Cyclooxygenase 2 Inhibitors : CK(464) : AC(272), Cyclooxygenase Inhibitors : CK( ... Pharmacological Actions : Cyclooxygenase Inhibitors : CK(71) : AC(39), Tumor Necrosis Factor (TNF) Alpha Inhibitor : CK(1823 ... 32 Curated Medical Research astracts associated with Cyclooxygenase Inhibitors. FRIEND membership. $8 / month $75 / year FRIEND ... Pharmacological Actions : Cyclooxygenase Inhibitors : CK(71) : AC(39), Postaglandin PGE2 downregulation : CK(23) : AC(11) ...
Two large pivotal trials have been published, in which the efficacy and safety of the COX 2 inhibitors celecoxib and rofecoxib ... Efficacy and safety of COX 2 inhibitors New data are encouraging but the risk:benefit ratio remains unclear ... with more specific inhibitory effects on cyclo-oxygenase 2 (COX 2) pathways, promised equivalent efficacy with greater safety ... Efficacy and safety of COX 2 inhibitors. BMJ 2002; 325 doi: (Published 21 September ...
Additional Keywords : Anticarcinogenic Agents, Cyclooxygenase 2 Inhibitors, NF-kappaB Inhibitor, Phloretin, skin cancer ... Additional Keywords : 5-Lipoxygenase Inhibitor, Anti-Inflammatory Agents, Cyclooxygenase 2 Inhibitors, Inflammation : CK(2) : ... Cyclooxygenase 2 Inhibitors : CK(1114) : AC(645), Interleukin-6 Downregulation : CK(3054) : AC(1144), NF-kappaB Inhibitor : CK( ... Cyclooxygenase 2 Inhibitors : CK(1114) : AC(645), Nitric Oxide Inhibitor : CK(390) : AC(196) ...
Their selectivity reduces the GI symptoms caused by inhibition of the COX-1 receptor. Despite some preliminary data su... more ... COX-2 specific inhibitors have also proven effective in relieving menstrual pain. ... What is the role of cyclooxygenase (COX) inhibitors in the treatment of dysmenorrhea?. Updated: Sep 23, 2019 ... COX-2 specific inhibitors have also proven effective in relieving menstrual pain. Their selectivity reduces the GI symptoms ...
Selective cyclooxygenase-2 (COX-2) inhibitors have provided relief for patients suffering from chronic pain and other ... We also touch on the COX-1/COX-2 selectivity of NSAIDs, the localization of COX enzymes in kidneys, and clinical studies ... NSAIDs and the kidney revisited: are selective cyclooxygenase-2 inhibitors safe?. Eras J1, Perazella MA. ... The documented reduction in gastric erosions, ulcerations, and perforations during the use of COX-2-selective inhibitors raises ...
COX 2 inhibitors, traditional NSAIDs, and the heart BMJ 2005; 330 :1342 doi:10.1136/bmj.330.7504.1342 ... COX 2 inhibitors, traditional NSAIDs, and the heart. BMJ 2005; 330 doi: (Published 09 ...
Cox-2 inhibitor definition at, a free online dictionary with pronunciation, synonyms and translation. Look it up ... cox-2 inhibitor in Medicine Expand. COX-2 inhibitor n. Any of a class of nonsteroidal anti-inflammatory drugs thought to have ...
COX-2 inhibitors are associated with increased risk of heart attack, heart failure and death from stroke. ... COX-2 inhibitors - are a type of "selective" nonsteroidal anti-inflammatory drug (NSAID). Examples of COX-2 inhibitors include ... history of COX-2 inhibitor use, including when they were using these drugs and what type of COX-2 inhibitors they were taking. ... COX-2 inhibitors linked to increased risk of stroke death. Written by David McNamee on November 6, 2014 ...
Very-low-birthweight preterm infants with thrombocytopenia treated with cyclooxygenase inhibitors are at an increased risk for ... Very-low-birthweight preterm infants with thrombocytopenia treated with cyclooxygenase (COX) inhibitors are at an increased ... For infants with a platelet count of at least 100 x 109/L, treatment of PDA with a COX inhibitor was not associated with an ... Although COX inhibitors are frequently used to treat patent ductus arteriosus (PDA), a common complication related to ...
The effect of celecoxib, a cyclooxygenase-2 inhibitor, in familial adenomatous polyposis.. Steinbach G1, Lynch PM, Phillips RK ... We studied the effect of celecoxib, a selective cyclooxygenase-2 inhibitor, on colorectal polyps in patients with familial ... a cyclooxygenase-2 inhibitor, leads to a significant reduction in the number of colorectal polyps. ... the chemopreventive effects of nonsteroidal antiinflammatory drugs may be related to their inhibition of cyclooxygenase-2. ...
To date, which COX isoform (COX-1 or COX-2) plays a more important role in during fetal development and influences kidney ... function early in life is not known, though evidence points to a predominant role for COX-2. Clinical implications of the use ... This review summarizes our current understanding of the role of cyclo-oxygenase inhibitors (COXI) in influencing the structural ... 2. COX Isoforms. Two main COX isoforms have been identified constitutive COX-1 and inducible COX-2, which catalyze the first ...
Two related isoforms of the cyclo-oxygenase (COX) enzyme have been described: COX-1 (PGHS-1) and COX-2 (PGHS-2). COX-1 is ... See COX-2 selective inhibitors: Adverse cardiovascular effects.). Other COX-2 inhibitors are available in some countries. ... to 300-fold selectivity for inhibition of COX-2 over COX-1. (See Overview of selective COX-2 inhibitors.) ... An overview of COX-2 inhibitors is also available. (See Overview of selective COX-2 inhibitors.) ...
Hypertension and Cyclooxygenase-2 Inhibitors. Target: The Renal Medulla. Chuan-Ming Hao, Matthew D. Breyer ...
Products are for research use only. Not for human use. We do not sell to patients.. © Copyright 2013 Selleck Chemicals. All Rights Reserved.. ...
... is one type of COX-2 inhibitor used to treat inflammation and back pain. This article includes information about potential side ... As a COX-2 inhibitor, celecoxib blocks an inflammation-promoting enzyme called COX-2. Medications known as COX-2 inhibitors ... See Understanding COX-2 Inhibitor Side Effects. Celebrex is still available, but with strong warnings, as are required for all ... See Safe Use of COX-2 Inhibitors and Other NSAIDs. However, many reports of heart attacks and stroke prompted the FDA to re- ...
Sponsors of other COX-2 inhibitors will also be asked for updated safety data, including details of any studies underway. ... The local pattern of use indicated that users of COX-2 inhibitors were older, had other co-morbidities and were often on ... Prescribers can assist in monitoring the safety of all COX-2 inhibitors by reporting adverse events to the Centre for Adverse ... What about the other COX-2 inhibitors?. At this stage, there is insufficient information available to comment on the ...
... it may be possible to continue the selective COX-2 inhibitor by reducing the dose of warfarin.2,3 Otherwise the COX-2 inhibitor ... If a COX-2 inhibitor is considered necessary for a patient taking warfarin, the INR should be checked a few days after ... The interaction between COX-2 inhibitors and warfarin has now been included in the list of adverse reactions of current concern ... The selective COX-2 inhibitors, celecoxib (Celebrex™) and rofecoxib (Vioxx™), may interact with warfarin causing an increase in ...
Cyclooxygenase (COX) inhibitors, such as indomethacin and ibuprofen, are often used for the treatment of PDA... ... Cyclooxygenase (COX) inhibitors, such as indomethacin and ibuprofen, are often used for the treatment of PDA in preterm infants ... Cyclooxygenase inhibitors Patent ductus arteriosus Preterm infant Predict Response This is a preview of subscription content, ... However, as observed in clinical practice, not all PDAs in preterm infants can be closed using COX inhibitors. Some studies ...
... a COX-2 selective inhibitor (celecoxib), and a nonselective COX inhibitor (piroxicam) for reducing catabolic MMP and PGE2 ... whereas COX-1 activity may have a more constitutive role in chondrocytes [14, 35]. We chose to investigate the COX-2 inhibitor ... a nonspecific COX inhibitor NSAID (piroxicam), or a COX-2 selective NSAID (celecoxib). Both prednisone and celecoxib decreased ... C. J. Hawkey, "COX-2 inhibitors," The Lancet, vol. 353, no. 9149, pp. 307-314, 1999. View at Publisher · View at Google Scholar ...
COX-2 inhibitors. Class Summary. Cyclooxygenase 2 (COX-2) inhibitors have a lower incidence of GI bleeding as compared with ... Inhibition of COX-1 may contribute to NSAID GI toxicity. At therapeutic concentrations, COX-1 isoenzyme is not inhibited, thus ... Primarily inhibits COX-2. COX-2 is considered an inducible isoenzyme, induced by pain and inflammatory stimuli. ... Their mechanism of action is not known, but they may inhibit cyclo-oxygenase activity and prostaglandin synthesis. Other ...
Cyclooxygenases catalyze the rate limiting step in the production of prostanoids. Accumulating data demonstrate that ... in particular the role of COX-2 will be highlighted. Finally, potential novel therapeutic molecular targets will be discussed. ... numerous studies show that inhibition of cyclooxygenases- 2 can delay or prevent certain forms of cancer. Aim of this review is ... overexpression of these enzymes, and in particular of cyclooxygenases- 2, promotes multiple events involved in tumorigenesis; ...
The co-administration of acetylsalicylic acid might reduce the safety advantage of COX-2s over that of nonselective NSAIDs. ... COX-2s appear to offer greater upper GI safety and are better tolerated than nonselective NSAIDs. ... Background & aims: Nonselective non-steroidal anti-inflammatory drugs (NSAIDs) and cyclooxygenase-2 inhibitors (COX-2s) are ... Gastrointestinal safety of cyclooxygenase-2 inhibitors: a Cochrane Collaboration systematic review Clin Gastroenterol Hepatol. ...
  • COX-2 inhibitors appear to work as well as nonselective NSAIDS. (
  • The impetus for development of selective COX-2 inhibitors was the adverse gastrointestinal side-effects of NSAIDs. (
  • Soon after the discovery of the mechanism of action of NSAIDs, strong indications emerged for alternative forms of COX, but little supporting evidence was found. (
  • Before the confirmation of COX-2 existence, the Dupont company had developed a compound, DuP-697, that was potent in many anti-inflammatory assays but did not have the ulcerogenic effects of NSAIDs. (
  • Enormous effort was spent on the development of NSAIDs between the 1960s and 1980 so there were numerous pharmacophores to test when COX-2 was discovered. (
  • Efforts have been made to convert NSAIDs into selective COX-2 inhibitors such as indometacin by lengthening of the alkylcarboxylic acid side-chain, but none have been marketed. (
  • Having spent the last two months reviewing the safety of the COX-2-selective non-steroidal anti-inflammatory drugs (NSAIDs), the US regulatory agency. (
  • Rofecoxib is one of the new breed of anti-inflammatories known as COX-2 (cyclo-oxygenase-2) inhibitors that are supposed to be safer than NSAIDs such as aspirin. (
  • But NSAIDs quickly became COX-2 inhibitors associated with adverse gastrointestinal effects such as peptic. (
  • Two large pivotal trials have been published, in which the efficacy and safety of the COX 2 inhibitors celecoxib and rofecoxib were compared with various traditional NSAIDs. (
  • Despite some preliminary data suggesting efficacy in patients with primary dysmenorrhea, COX-2 inhibitors have not been demonstrably superior to conventional NSAIDs. (
  • NSAIDs and the kidney revisited: are selective cyclooxygenase-2 inhibitors safe? (
  • In addition, studies evaluating the renal effects of the selective nonsteroidal anti-inflammatory drugs (NSAIDs) are inconclusive, and available data on the renal effects of COX-2-selective inhibitors are conflicting. (
  • Therefore, this article reviews the role of cyclooxygenase enzyme activity and associated prostaglandins in the kidney and the adverse renal effects of nonselective NSAIDs. (
  • We also touch on the COX-1/COX-2 selectivity of NSAIDs, the localization of COX enzymes in kidneys, and clinical studies examining the renal effects of selective COX-2 inhibitors. (
  • Because COX enzymes are the rate-limiting step in the aforementioned cascade, the generation of PGs can be inhibited by the administration of COX inhibitors (COXI) collectively known as non- steroidal anti-inflammatory drugs (NSAIDs) [ 10 ]. (
  • This topic review will summarize the major clinical trials that have focused on the gastroduodenal protective effects of the COX-2 inhibitors as compared to nonselective NSAIDs. (
  • Medications known as COX-2 inhibitors were developed to work as well as traditional NSAIDs but with fewer stomach problems. (
  • This requires consideration of both the adverse event profile of possible substitutes (such as NSAIDs or other COX-2 inhibitors) and patients' individual risk factors for gastrointestinal and cardiovascular harm. (
  • Patients with osteoarthritis (OA), a condition characterized by cartilage degradation, are often treated with steroids, nonsteroidal anti-inflammatory drugs (NSAIDs), and cyclooxygenase-2 (COX-2) selective NSAIDs. (
  • The anti-inflammatory effects of NSAIDs are mainly due to their ability to inhibit cyclooxygenase (COX), impairing production of prostaglandins, which are important mediators of both pain and the inflammatory response. (
  • Beneficial effects of NSAIDs on inflammation are mediated by COX-2 inhibition, whereas unwanted gastrointestinal effects are caused by primarily inhibition of COX-1 [ 12 ]. (
  • Cyclooxygenase 2 (COX-2) inhibitors have a lower incidence of GI bleeding as compared with other NSAIDs, although there is still a risk involved. (
  • At therapeutic concentrations, COX-1 isoenzyme is not inhibited, thus incidence of GI toxicity, such as endoscopic peptic ulcers, bleeding ulcers, perforations, and obstructions, may be decreased when compared to nonselective NSAIDs. (
  • Nonselective non-steroidal anti-inflammatory drugs (NSAIDs) and cyclooxygenase-2 inhibitors (COX-2s) are used to treat a variety of arthritic and inflammatory conditions. (
  • The aim of this study was to assess the upper gastrointestinal (GI) harms of the long-term use of COX-2s, compared with nonselective NSAIDs and placebo, in arthritis sufferers. (
  • RCTs of celecoxib, rofecoxib, etoricoxib, valdecoxib, and lumiracoxib were included if they reported on endoscopic ulcers, clinically important ulcer complications, or adverse gastrointestinal (GI) symptoms with the use of these COX-2s, compared with placebo or with nonselective NSAIDs. (
  • COX-2s appear to offer greater upper GI safety and are better tolerated than nonselective NSAIDs. (
  • The co-administration of acetylsalicylic acid might reduce the safety advantage of COX-2s over that of nonselective NSAIDs. (
  • NSAIDs suppress cyclooxygenase-2 (COX-2), which affects epithelial proliferation and apoptosis. (
  • If you use painkillers such as ibuprofen and other nonsteroidal anti-inflammatory drugs (NSAIDs) or COX-2 inhibitors to treat inflammation, you may be at increased risk of irregular heart rhythm, or atrial fibrillation. (
  • Before now, no study had explored whether NSAIDs and COX-2 inhibitors could increase the risk of this disorder. (
  • Investigators looked at their use of six commonly used painkillers: non-aspirin NSAIDS (ibuprofen, naproxen) and both older (diclofenac, etodolac) and newer (celecoxib, rofecoxib) COX-2 inhibitors. (
  • Patients and controls were classified based on their use of NSAIDs and COX-2 inhibitors: no use, recent use, current use (those who got their first prescription within 60 days of their diagnosis), long-term use, and new use. (
  • The increased risk differed depending on the drugs used: there was about a 40 percent increased risk for those who used non-selective NSAIDs and 70 percent among those who used COX-2 inhibitors. (
  • Both non-selective NSAIDS and COX-2 inhibitors have been associated with a number of side effects (e.g., gastrointestinal problems) and serious long-term risks, including an increased chance of a stroke and heart attack. (
  • Conventional treatment for these debilitating conditions routinely involves the use of conventional nonsteroidal anti-inflammatory drugs (NSAIDs), which are nonspecific inhibitors of COX-1 and COX-2. (
  • Recently developed non-steroidal anti-inflammatory drugs (NSAIDS) are targeted to inhibit COX-2 and treat inflammation and arthritic pain. (
  • It is thought that the therapeutic effects of these agents are related to the inhibition of COX-2 at sites of inflammation whereas the adverse gastrointestinal effects and bleeding associated with NSAIDs are attributed to inhibition of COX-1 in gastric epithelium and in platelets, respectively ( 27 ). (
  • COX-2 selective inhibitors are a new class of nonsteroidal anti-inflammatory drugs, or NSAIDs that directly targets the COX-2 enzyme. (
  • Because they selectively block the COX-2 enzymeâ€"the enzyme responsible for inflammation and painâ€"and not the COX-1 enzyme, these drugs are uniquely different from traditional NSAIDs. (
  • Dr. Blanke said that numerous studies have assessed the effects on the development of colorectal cancer of a wide variety of nonsteroidal anti-inflammatory drugs (NSAIDS), which inhibit COX-2, and acetaminophen. (
  • To determine whether race is a predictor of a patient's likelihood of being prescribed selective cyclooxygenase-2 inhibitors (COX-2s) versus other nonsteroidal anti-inflammatory agents (NSAIDs) in Medicaid managed care plans (MCO). (
  • Cox-2 inhibitors are non-steroidal anti-inflammatory drugs (NSAIDs) which selectively inhibit cyclooxygenase-2. (
  • The traditional NSAIDs inhibit both cyclooxygenase 1 and 2 (Cox-1 and Cox-2). (
  • The development of the Cox-2 selective inhibitors was intended to provide drugs that would offer the same pain relieving and anti-inflammatory effects as the traditional NSAIDs without causing the gastric ulcers that have been associated with the older drugs. (
  • Traditional NSAIDs inhibit the constitutional cyclooxygenase-1 (COX-1) enzyme responsible for eicosanoids biosynthesis not only in joints, a beneficial effect, but also in the stomach, a detrimental effect. (
  • Selective NSAIDs were specifically designed to preferentially inhibit the cyclooxygenase-2 (COX-2), an inducible enzyme mediating the production of inflammatory eicosanoids in the joints but sparing the endogenous protective eicosanoids in the stomach. (
  • Additional comprehensive, long-term, prospective investigations comparing the CV and GI safety profile of marketed NSAIDs against each other and against selective inhibitors are needed to address the controversy of COX inhibitors. (
  • The efficacy and toxicity of NSAIDs is a consequence of the inhibition of the COX enzymes [2]. (
  • Such important findings led to the development and subsequent introduction of the selective COX-2 inhibitors celecoxib, valdecoxib and rofecoxib, which have considerably reduced GI ulcerogenicity potential when compared with the older, non-selective NSAIDs [5]. (
  • The introduction of selective cyclooxygenase-2 (COX-2) inhibitors, a group of NSAIDs, has resulted in a rapid increase in the number of people exposed to NSAIDs. (
  • Many patients who would otherwise not have used an NSAID are now using COX-2 inhibitors without a corresponding decrease in the use of more traditional nonselective NSAIDs. (
  • 1 , 2 Although COX-2 inhibitors have been found to be associated with a lower risk of significant adverse gastrointestinal events than have traditional nonselective NSAIDs at the level of the individual patient, 3 , 4 recent evidence suggests that the market expansion created by COX-2 inhibitors may increase rates of hospital admissions because of upper gastrointestinal (GI) bleeding at the population level. (
  • For example, COX-2 inhibitors were listed in the Ontario Drug Benefit (ODB) formulary in April 2000 as limited-use drugs, which means that prescribers must indicate that the recipient has failed a trial of at least 3 nonselective NSAIDs or has clinically significant GI disease. (
  • The prevalence of NSAID use in each interval was determined by dividing the unique number of people dispensed any NSAID (either nonselective NSAIDs or COX-2 inhibitors) by the total number of people alive at the beginning of the interval. (
  • Cyclooxygenase-1 (Cox-1) is constitutively expressed in most tissues and is thought to serve in general "housekeeping" functions, and is a target for nonsteroidal therapeutic anti-inflammatory drugs (NSAIDs). (
  • 45% of the patients had received traditional non-steroidal anti-inflammatory drugs (NSAIDs), and 10% had received COX-2 inhibitors. (
  • The report authors concluded that even though COX-2 drugs were designed to provide pain relief without the serious gastrointestinal side-effects associated with conventional NSAIDs, 'we found no consistent evidence of enhanced safety against gastrointestinal events with any of the new cyclo-oxygenase-2 inhibitors [cox-2 inhibitors], compared with non-selective, nonsteroidal, anti-inflammatory drugs. (
  • Background- The selective cyclooxygenase-2 (COX-2) inhibitors and other nonselective nonsteroidal antiinflammatory drugs (NSAIDs) have been associated with increased cardiovascular risk, but the risk in patients with established cardiovascular disease is unknown. (
  • We analyzed the risk of rehospitalization for acute myocardial infarction (MI) and death related to the use of NSAIDs including selective COX-2 inhibitors in patients with prior MI. (
  • The risk of death and rehospitalization for MI associated with the use of selective COX-2 inhibitors and nonselective NSAIDs was studied with the use of multivariable proportional hazards models and case-crossover analysis. (
  • There were trends for increased risk of rehospitalization for MI associated with the use of both the selective COX-2 inhibitors and the nonselective NSAIDs. (
  • Conclusions- Selective COX-2 inhibitors in all dosages and nonselective NSAIDs in high dosages increase mortality in patients with previous MI and should therefore be used with particular caution in these patients. (
  • Little is known about the extent to which the cardiovascular risk of selective COX-2 inhibitors relates to this population and whether other nonselective NSAIDs are also associated with increased risk. (
  • Therefore, we used nationwide administrative registers of hospitalization and drug dispensing from pharmacies in Denmark to study the risk of recurrent MI and death related to the use of selective COX-2 inhibitors and nonselective NSAIDs in patients discharged after first-time acute MI between 1995 and 2002. (
  • In recent studies, the cyclooxygenase-2 (COX-2) inhibitor rofecoxib demonstrated analgesic effects similar to those of NSAIDs in the treatment of acute pain and primary dysmenorrhea. (
  • Use of cyclo-oxygenase 2 inhibitors (COX-2) and prescription non-steroidal anti-inflammatory drugs (NSAIDS) in UK and USA populations. (
  • BACKGROUND: COX-2 and NSAIDS differ in their gastrointestinal (GI) and cardiovascular (CV) toxicity from pharmacological, clinical and epidemiologic point of views. (
  • OBJECTIVE: Describe the patterns of use of NSAIDS and COX-2 in The Health Improvement Network (THIN) database in UK and the PharMetrics database in USA. (
  • Diclofenac and ibuprofen (NSAIDS), and celecoxib and rofecoxib (COX-2) were the agents prescribed most frequently. (
  • More COX-2 users than NSAIDS users received concomitant gastroprotective agents (GPA), corticosteroids and anti-platelet therapy, and had a history of thromboembolic events and hypertension. (
  • PharMetrics patients were prescribed higher doses of NSAIDS and COX-2. (
  • However, one must ask why would we choose selective COX-2 inhibitors instead of conventional non-steroidal anti-inflammatory drugs (NSAIDs) for patients taking anti-platelet therapy? (
  • A most promising approach seemed to be the preparation of novel NSAIDs, specific for the inducible isoform of cyclooxygenase (COX-2): they appear to be devoid of gastrointestinal toxicity, in that they spare mucosal prostaglandin synthesis. (
  • Moreover, COX-2 selective NSAIDs have lost the cardiovascular protective effects of non-selective NSAIDs, effects which are mediated through COX-1 inhibition (in addition, COX-2 has a role in sustaining vascular prostacyclin production). (
  • Non-steroidal anti-inflammatory drugs (NSAIDs) have potentially dangerous side effects, which has led to intense interest in the development of the cyclo-oxygenase (COX) inhibitors. (
  • As an alternative to NSAIDs, selective cyclooxygenase 2 (COX-2) inhibitors were developed to improve tolerability (i.e. the degree to which the side effects of a drug can be tolerated by a patient). (
  • FARMINGTON, CONN. Careful monitoring and control of blood pressure are key when NSAIDS or COX-2 inhibitors are used for osteoarthritis management for patients with hypertension and type 2-diabetes, according to a study published in the January 24 issue of Archives of Internal Medicine . (
  • This is because both COX-1 and COX-2 enzymes are inhibited to varying degrees by all currently available (1st generation) NSAIDs. (
  • Studies published so far support the hypothesis that the undesirable side effects of NSAIDs such as gastric erosion and renal dysfunction are due to the inhibition of COX-1 enzymes, while the anti-inflammatory (therapeutic) effects are due to the inhibition of COX-2 enzymes. (
  • Here is the key: Inhibitory potency and selectivity of the conventional, 1st generation NSAIDs for COX-1 and COX-2 enzymes vary greatly. (
  • Some NSAIDs (e.g., ketoprofen) are relatively COX-1 selective, some (ibuprofen and naproxen) are essentially non-selective, while others (e.g., diclofenac) are relatively COX-2 selective. (
  • A new type of NSAID, called cyclooxygenase-2 (COX-2) inhibitors, affects some important body processes less than do earlier NSAIDs (COX-1/COX-2 inhibitors). (
  • THU0182 Significant reduction in serious upper gastrointestinal (ugi) events with celecoxib, a cox-2 specific inhibitor, compared with conventional nsaids. (
  • The inhibition of COX-2 is paramount for the anti-inflammatory and analgesic function of the selective COX-2 inhibitor celecoxib. (
  • However, with regard to this drug's promise for the therapy of advanced cancers, it is unclear whether the inhibition of COX-2 plays a dominant role, and this has become a controversial and intensely researched issue. (
  • However, when the ability of all these compounds to kill tumor cells in cell culture was investigated, it turned out that the antitumor potency did not at all depend on whether or not the respective compound could inhibit COX-2, showing that inhibition of COX-2 was not required for the anticancer effects. (
  • As of 2012 results have been converging on the hypothesis that the adverse cardiovascular effects are most likely due to inhibition of COX-2 in blood vessels, which leads to a decrease in the production of prostacyclin in them. (
  • Their selectivity reduces the GI symptoms caused by inhibition of the COX-1 receptor. (
  • By contrast, for those with moderately decreased platelets (50-99 x 10 9 /L), COX inhibition amplified the risk for bleeding on days 2 to 7 more than 50-fold compared with infants with a platelet count of at least 100 x 10 9 /L who received no treatment. (
  • In this disease, the chemopreventive effects of nonsteroidal antiinflammatory drugs may be related to their inhibition of cyclooxygenase-2. (
  • These drugs have at least a 200- to 300-fold selectivity for inhibition of COX-2 over COX-1. (
  • Kim ES, Kim EK, Choi CW et al (2010) Intrauterine inflammation as a risk factor for persistent ductus arteriosus patency after cyclooxygenase inhibition in extremely low birth weight infants. (
  • Inhibition of COX-1 may contribute to NSAID GI toxicity. (
  • in addition, numerous studies show that inhibition of cyclooxygenases- 2 can delay or prevent certain forms of cancer. (
  • Three small studies (102 women), two of which were conducted in the 1980's, compared COX inhibition (indomethacin only) with placebo. (
  • The mechanism of NSAID-induced polyp regression is not completely known, but it thought that it is at least in part due to inhibition of cyclooxygenase 2 (COX2) and the resultant decrease in prostaglandin synthesis although a non-COX mechanism may also contribute. (
  • There was no significant difference between the doses of celecoxib on COX-2 inhibition. (
  • Given this background, attempts to combine COX-2 inhibition with chemotherapy constitute a logical next step. (
  • The effects of COX-2 inhibition and radiation are synergistic, and treatment increases the actual cure rate. (
  • COX-2 overexpression is independently associated with disease-free survival, and COX-2 inhibition might be useful in preventing hematogenous metastasis,' he said. (
  • Selective COX-2 inhibition enhances mitomycin-C-induced apoptosis,' Dr. Blanke said. (
  • Clinical trials should incorporate COX-2 inhibition into treatment regimens,' he concluded. (
  • In order to gain insight into the anticancer activity and COX-2 inhibition, molecular docking studies were carried out for COX-1 and COX-2 enzymes utilizing the newly synthesized compounds 15 , and 16 . (
  • Epidemiological and laboratory studies suggest that nonsteroidal anti-inflammatory drugs reduce the risk of colon cancer and that the inhibition of colon carcinogenesis is mediated through modulation of prostaglandin production by cyclooxygenase (COX) isozymes (COX-1 and -2). (
  • We tested this hypothesis by studying whether an inhibition of the rate-limiting enzyme of prostaglandin biosynthesis, cyclooxygenase (COX), caused developmental disturbances analogous to those seen in embryos exposed to high glucose concentration. (
  • This effect was found to be due to inhibition of COX-2 enzyme activity by chamomile. (
  • Our study aimed to demonstrate the potential and mechanisms of TP as an anti-inflammation action without the side effects of COX-1 inhibition. (
  • The anti-inflammatory effects of TP can possibly regulate macrophages due to the targeted inhibition of COX-2 activity, without affecting COX-1 activity with other anti-inflammatory effects including suppression of iNOS and inflammatory cytokines. (
  • COX-2 inhibition with celecoxib is an effective approach for the treatment of osteoarthritis , as seen by clinical improvement in signs and symptoms comparable to treatment with naproxen . (
  • However, several lines of evidence suggest that mechanisms of COX-2 inhibitor beyond the inhibition of COX and PG biosynthesis might also play an important role in their antinociception. (
  • Rofecoxib is a time-dependent inhibitor of purified human recombinant COX-2 (IC 50 = 0.34 μM) but caused inhibition of purified human COX-1 in a non-time-dependent manner that could only be observed at a very low substrate concentration (IC 50 = 26 μM at 0.1 μM arachidonic acid concentration). (
  • In an in vitro human whole blood assay, rofecoxib selectively inhibited lipopolysaccharide-induced, COX-2-derived PGE 2 synthesis with an IC 50 value of 0.53 ± 0.02 μM compared with an IC 50 value of 18.8 ± 0.9 μM for the inhibition of COX-1-derived thromboxane B 2 synthesis after blood coagulation. (
  • COX inhibitors and β-blockers were recently suggested to reduce cancer progression through inhibition of tumor proliferation and growth factor secretion, induction of tumor apoptosis, and prevention of cellular immune suppression during the critical perioperative period. (
  • COX-2 inhibition, but not COX-1 inhibition, reduced postoperative LTR. (
  • Treatment combining perioperative COX-2 inhibition and β-blockade is practical in operated cancer patients, and our study suggests potential immunological and clinical benefits. (
  • Cyclooxygenase-2 inhibition induces apoptosis signaling via death receptors and mitochondria in hepatocellular carcinoma. (
  • The summary below is from the full report titled "Effect of Cyclooxygenase-2 Inhibition on Renal Function in Elderly Persons Receiving a Low-Salt Diet. (
  • The aim of the study was to determine the effect of aromatase and/or COX-2 inhibition on epithelial proliferation and apoptosis in a presurgical study of estrogen receptor (ER)-positive DCIS. (
  • Inhibition of DCIS epithelial proliferation by exemestane in a placebo-controlled trial provides proof of principle that aromatase inhibitors will do likewise in the current ongoing adjuvant trials in DCIS. (
  • It has become apparent that cyclooxygenase (COX)-2 plays an important role in cancer growth, invasion and metastasis and that there is potential for chemoprevention via inhibition of these processes. (
  • In the present study, we investigated the effects of selective inhibition of COX-2 with nimesulide (12 mg/kg) and selective inhibition of COX-1 with valeryl salicylate (VAS, 12-120 mg/kg) on prostaglandin E2 (PGE2) levels, myeloperoxidase (MPO) activity, Evans Blue (EB) extravasation and infarct volume in a standardized model of transient focal cerebral ischemia in the rat. (
  • These studies provide the first experimental evidence that COX-2 inhibition with nimesulide is able to limit BBB disruption and leukocyte infiltration following transient focal cerebral ischemia. (
  • On the other hand, selective inhibition of COX-1 with VAS had no significant effect on the evaluated parameters. (
  • These data suggest that COX-2 activity, but not COX-1 activity, contributes to the progression of focal ischemic brain injury, and that the beneficial effects observed with non-selective COX inhibitors are probably associated to COX-2 rather than to COX-1 inhibition. (
  • Targeting selectivity for COX-2 reduces the risk of peptic ulceration , and is the main feature of celecoxib , rofecoxib and other members of this drug class. (
  • Celecoxib and rofecoxib, the first COX-2 inhibitors to reach market, were based on DuP-697. (
  • It took less than eight years to develop and market the first COX-2 inhibitor, with Celebrex (celecoxib) launched in December 1998 and Vioxx (rofecoxib) launched in May 1999. (
  • Concerns about the potential prothrombotic effects of COX-2 inhibitors first arose with rofecoxib (Vioxx® - Merck) in the Vioxx Gastrointestinal Outcomes Research (VIGOR) trial, when the rate of MIs in patients taking rofecoxib was higher than in those taking the comparator NSAID naproxen . (
  • Examples of COX-2 inhibitors include older drugs such as diclofenac, etodolac, nabumeton and meloxicam, and newer drugs like celecoxib and rofecoxib. (
  • Rofecoxib is a COX-2 inhibitor that was removed due to an increased risk of stroke and myocardial infarction with long-term use. (
  • From the date of first marketing, Medsafe (and other regulatory agencies around the world) have collected and analysed adverse reaction reports for rofecoxib and the other COX-2 inhibitors as part of standard post-marketing monitoring practice. (
  • Medsafe will be asking the MARC to determine whether the risk of cardiovascular events is similar for the other COX-2 inhibitors, in comparison to rofecoxib. (
  • The selective COX-2 inhibitors, celecoxib ( Celebrex ™) and rofecoxib (Vioxx™), may interact with warfarin causing an increase in the international normalised ratio (INR) and putting the patient at risk of a haemorrhagic event. (
  • If celecoxib or rofecoxib are considered necessary for a patient taking warfarin, the INR should be checked a few days after introduction of the COX-2 inhibitor and monitored closely for the first two weeks. (
  • The newer arthritis drugs such as rofecoxib, and celecoxib, inhibit the COX-2 form of the enzyme, and reduce pain without causing a high incidence of gastric erosion. (
  • However, a French review warned that certain selective Cox-2 inhibitors (i.e. celecoxib, rofecoxib) have not been tested for safety on patients with ulcers or cardiovascular or renal disease. (
  • The availability of the COX-2-specific inhibitor (CSI) class of anti-inflammatory drugs, namely celecoxib and rofecoxib, has raised a number of questions. (
  • The risk was significantly higher for the COX-2 inhibitors naproxen, and rofecoxib (Vioxx), and diclofenac (Voltaren). (
  • 5-14 This caused the pharmaceutical company Merck to withdraw their COX-2 inhibitor rofecoxib (Vioxx) from the market, and health authorities in several countries have issued a warning about the cardiovascular risk associated with the use of COX-2 inhibitors. (
  • The present randomized, single-dose, double-blind, double-dummy, placebo- and active-comparator-controlled, parallel-group study was undertaken to compare the analgesic efficacy of the COX-2 inhibitors rofecoxib 50 mg and celecoxib 200 mg with that of ibuprofen 400 mg and placebo in patients with postoperative dental pain. (
  • In the present study, the preclinical pharmacological and biochemical profiles of rofecoxib [Vioxx, also known as MK-0966, 4-(4′-methylsulfonylphenyl)-3-phenyl-2-( 5H )-furanone], an orally active COX-2 inhibitor, are described. (
  • In several in vivo rodent models, rofecoxib is a potent inhibitor of carrageenan-induced paw edema (ID 50 = 1.5 mg/kg), carrageenan-induced paw hyperalgesia (ID 50 = 1.0 mg/kg), lipopolysaccharide-induced pyresis (ID 50 = 0.24 mg/kg), and adjuvant-induced arthritis (ID 50 = 0.74 mg/kg/day). (
  • Rofecoxib is a novel COX-2 inhibitor with a biochemical and pharmacological profile clearly distinct from that of current nonsteroidal anti-inflammatory drugs and represents a new therapeutic class of anti-inflammatory agents for the treatment of the symptoms of osteoarthritis and rheumatoid arthritis with improved gastrointestinal tolerability. (
  • This review does not include any studies that assessed the tolerability and safety of the withdrawn COX-2 inhibitors rofecoxib, valdecoxib, or lumiracoxib.This review identified two studies that included a total of 381 participants with IBD who were experiencing rheumatological manifestations. (
  • The Celecoxib Rofecoxib Efficacy and Safety in Comorbodities Evaluation Trial, or Crescent, evaluated the effects of the COX-2 inhibitors and naproxen on 24-hour blood pressure reading in patients with type-2 diabetes, hypertension, and osteoarthritis. (
  • This suggests that COX-2 inhibitors (for example, rofecoxib) may cause fewer side effects in patients than COX-1/COX-2 inhibitors (for example, ibuprofen and indomethacin). (
  • To see if the COX-2 inhibitor rofecoxib affects kidney function. (
  • Patients in both parts of the study had reversible decreases in kidney function with the COX-2 inhibitor (rofecoxib) that were similar to those with the COX-1 inhibitor (indomethacin). (
  • Selective COX-2 inhibitors are a type of nonsteroidal anti-inflammatory drug (NSAID) that directly targets cyclooxygenase-2, COX-2 , an enzyme responsible for inflammation and pain . (
  • Cox-2 Inhibitors are nonsteroidal anti-inflammatory drugs used to relieve pain and inflammation. (
  • Bacopa reduces inflammation by positively modulating COX and LOX enzyme pathways and Tumor Necrosis Factor. (
  • It had been proposed that the ideal NSAID would inhibit the inducible COX-2 isoform (thereby decreasing inflammation) without having any effect on the constitutive COX-l isoform (thereby minimizing gastric toxicity) [ 1 ]. (
  • As a COX-2 inhibitor, celecoxib blocks an inflammation-promoting enzyme called COX-2. (
  • These agents inhibit COX-2, thus suppress production of prostaglandin E2 at inflammation sites. (
  • While inflammation has been shown to be a factor in many forms of cancer, the researchers say this is the first study to demonstrate the effect of an anti-inflammatory COX-2 inhibitor on the development of pancreatic cancer. (
  • COX-2, an enzyme which causes inflammation, is no stranger to cancer researchers. (
  • More particularly, the invention provides a combination therapy for the treatment of pain, inflammation or inflammation mediated disorders comprising the administration to a subject of a potassium ion channel modulator in combination with a cyclooxygenase-2 selective inhibitor. (
  • Joint inflammation and pain such as that associated with osteoarthritis is the result of increased levels of pro-inflammatory prostaglandins that are derived from arachidonic acid via the enzyme cyclooxygenase. (
  • Inflammation in arthritic joints involves an enzyme called cyclooxogenase, or "Cox," that starts the biochemical pathway leading to swelling, stiffness and pain. (
  • The biologically active ingredient, curcumin, is an anti-inflammatory compound that inhibits the activity of cyclooxygenase and other enzymes that cause inflammation, according to the Linus Pauling Institute at Oregon State University. (
  • A number of studies support use of turmeric or purified curcumin to inhibit Cox activity and suppress inflammation. (
  • According to Memorial Sloan-Kettering Cancer Center, bromelian may have anti-inflammatory activity due to its ability to reduce levels of prostaglandin, a compound that is increased by Cox activity and that causes inflammation. (
  • COX-2 specific inhibitors are thought to relieve pain and inflammation by targeting the COX-2 enzyme. (
  • Unlike ketorolac, which affects both COX-1 and COX-2, COX-2-specific inhibitors like parecoxib are less likely to cause GI ulceration or promote bleeding, while still effectively reducing pain and inflammation. (
  • COX-2 inhibitors are newly developed drugs for inflammation that selectively block the COX-2 enzyme. (
  • Blocking the COX-2 enzyme stops the production of the chemical messengersâ€"or prostaglandinsâ€"that cause the pain and swelling of arthritis inflammation. (
  • Apart from their relation with inflammation, the additional involvement of COX-2 enzyme with cancer activity was recently discovered. (
  • The constitutive COX-1 isoenzyme which can be found throughout the body, where it is responsible for the protection of the gastrointestinal track, whereas COX-2 is an inducible isoenzyme responsible for inflammation [ 1 , 2 ]. (
  • However, while Cox-2 is associated with inflammation and pain , Cox-1 maintains the integrity of the gastric mucosa, mediates normal platelet function, and regulates renal blood flow. (
  • Cox Inhibitors offered by Santa Cruz inhibit Cox and, in some cases, other prostaglandin and inflammation related proteins. (
  • Inducible cyclooxygenase (COX-2) has been implicated in the process of inflammation and carcinogenesis. (
  • Comparative protection against liver inflammation and fibrosis by a selective cyclooxygenase-2 inhibitor and a nonredox-type 5-lipoxygenase inhibitor. (
  • In this study, we examined the relative contribution of cyclooxygenase-2 (COX-2) and 5-lipoxygenase (5-LO), two major proinflammatory pathways up-regulated in liver disease, to the progression of hepatic inflammation and fibrosis. (
  • Taken together, these findings indicate that both COX-2 and 5-LO pathways are contributing factors to hepatic inflammation and fibrosis and that these two pathways of the arachidonic acid cascade represent potential targets for therapy. (
  • However, a number of recent studies raised serious questions about the two central tenets that support this approach, namely that the prostaglandins that mediate inflammation and pain are produced solely via COX-2 and that the prostaglandins that are important in gastrointestinal and renal function are produced solely via COX-1. (
  • So, increasing evidence shows that COX-2 (not only COX-1) also plays a physiological role in several body functions and that, conversely, COX-1 (not only COX-2) may also be induced at sites of inflammation. (
  • The discoveries that cyclooxygenase (COX)-2 is an inducible form of COX involved in inflammation and that COX-1 is the major isoform responsible for the production of prostaglandins (PGs) in the gastrointestinal tract have provided a rationale for the development of specific COX-2 inhibitors as a new class of anti-inflammatory agents with improved gastrointestinal tolerability. (
  • Herbs that directly target COX-2, an enzyme responsible for inflammation and pain, are often used to treat long term pain and arthritis. (
  • The re-emergence, in the recent years, of cyclooxygenase as a biological target in therapeutic areas other than inflammation is likely to require new optimized leads, particularly suited for the requirements of specific drug development programs. (
  • The COX-2 enzyme was discovered in 1988 by Daniel Simmons, a Brigham Young University researcher. (
  • COX enzyme proved to be difficult to purify and was not sequenced until 1988. (
  • In 1991 the existence of the COX-2 enzyme was confirmed by being cloned by Dr. Dan Simmons at Brigham Young University. (
  • Once the COX-2 enzyme was identified, Dup-697 became the building-block for synthesis of COX-2 inhibitors. (
  • In 1991, during the investigation of the expression of early-response genes in fibroblasts transformed with Rous sarcoma virus, a novel mRNA transcript that was similar, but not identical, to the seminal COX enzyme was identified. (
  • The same laboratory showed that this gene truly expressed a novel COX enzyme. (
  • The two enzymes were renamed COX-1, referring to the original enzyme and COX-2. (
  • In vitro recombinant enzyme assays provided powerful means for assessing COX selectivity and potency and led to the discovery and clinical development of the first rationally designed COX-2 selective inhibitor, celecoxib. (
  • Scientists have succeeded in reducing levels of the bovine leukemia virus in cows with severe infections by combining an immune checkpoint inhibitor and an enzyme inhibitor. (
  • The cyclooxygenase-2 enzyme is just such a protein, as the concentration of COX-2 is greater in cancer cells than in adjacent normal tissues. (
  • However, kidney tissue seems to possess "constitutive" or homeostatic COX-2 enzyme, suggesting a role for prostaglandins produced by this isoform. (
  • The study found that the COX-2 enzyme is mostly found just in the brain, gut, kidney and thymus gland. (
  • Cyclo-oxygenase (COX) is a rate limiting enzyme in the generation of the important family known as prostaglandins (PGs). (
  • Two related isoforms of the cyclo-oxygenase (COX) enzyme have been described: COX-1 (PGHS-1) and COX-2 (PGHS-2). (
  • There are two isoforms of the COX enzyme: COX-1, found in most tissues and constitutively expressed in normal cells, and COX-2, which is not expressed in healthy tissue but is induced by various catabolic mediators, such as cytokines, growth factors, and mechanical stress [ 11 ]. (
  • There are two types of this enzyme, COX-1 and COX-2. (
  • Non-steroidal anti-inflammatory drugs such as aspirin and ibuprofen reduce the pain and swelling of arthritis by inhibiting the COX-1 form of the enzyme, but have the side effect of causing gastric erosion if used on a regular basis. (
  • Furthermore, there was no evidence of drug-drug interactions between celecoxib and concomitant angiotensin-converting enzyme (ACE) inhibitors, beta-blockers, calcium channel blockers, or diuretics. (
  • Cyclo-oxygenase-2 (COX-2) is a key enzyme in the production of prostaglandins (PG), and evidence suggests that COX-2 plays an important role in the pathogenesis of acute lung injury (ALI). (
  • More interestingly, this effect is independent of the COX-2 enzyme. (
  • In some cancer types the level of COX-2 enzyme is increased indicating that this enzyme could be a suitable target for cancer therapy. (
  • Recent research has disclosed at least two types of COX enzymes exits: COX-1 is a constitutive enzyme responsible for housekeeping functions in organs such as the stomach, kidney, intestine and platelets, while COX-2 is an inducible enzyme exerting its action at inflammatory sites of the joints and muscles [3,4]. (
  • COX-2 syntheses prostaglandin (PG) E 2 , which is a species of endogenous pain-producing substance, whereas COX-1 acts as a house-keeping enzyme. (
  • COX inhibitor screening assay showed TP as a selective inhibitor of COX-2 enzyme. (
  • Cyclooxygenase (COX) is an enzyme naturally present in our body. (
  • Scientists discovered there were two forms of this Cyclooxygenase COX enzyme -- COX-1 and COX-2 enzymes. (
  • Simply put, by continually having an unbalanced fatty acid intake we are giving the COX-2 enzyme the raw material to create fire, but not the raw material to put out the fire. (
  • No, as mentioned previously, COX-2 enzyme production occurs due to a myriad of factors and COX-2 production does not indicate that you are in a state of disease. (
  • Hence, the introduction of dietary modifications that inhibit the COX-2 enzyme. (
  • So, even though research is examining the role of excessive COX-2 enzyme production as a factor, healthy individuals can experience COX-2 enzyme production in amounts higher than normal, whether it is from diet, trauma or stress, or foreign invaders. (
  • Previous research has linked the cyclooxygenase-2 enzyme commonly. (
  • Previous research has linked the cyclooxygenase-2 enzyme, commonly known as COX-2, to many cancer types, including prostate cancer, said Mukhtar. (
  • The drugs assessed in the study - COX-2 inhibitors - are a type of "selective" nonsteroidal anti-inflammatory drug ( NSAID ). (
  • One NSAID that selectively inhibits COX-2, celecoxib, is currently approved by the US Food and Drug Administration (FDA). (
  • The chondrocytes were then treated with either a steroid (prednisone), a nonspecific COX inhibitor NSAID (piroxicam), or a COX-2 selective NSAID (celecoxib). (
  • Of 9407 cases, 45% had been prescribed a conventional non-steroidal anti-inflammatory drug (NSAID) in the previous three years and 10% had been prescribed a COX-2 inhibitor. (
  • Of 88,867 controls, 33% had been prescribed an NSAID and 6% had been prescribed a COX-2 inhibitor. (
  • As celecoxib inhibits COX-2 and spares COX-1 at therapeutic doses, we hypothesized that it may offer an improved renal safety profile in patients at risk for NSAID-induced renal toxicity. (
  • All medical and prescription claims for Medicaid MCO enrollees receiving at least one prescription for a COX-2 or NSAID between January 2000 and June 2002 were retrieved. (
  • Of the 16,868 enrollees meeting the selection criteria, 4,005 (24%) were prescribed a COX-2 and 12,863 another NSAID. (
  • These differences in the nature and timing of reimbursement for COX-2 inhibitors have contributed to vastly different rates of NSAID use at the population level. (
  • To explore this issue further, we conducted a population-based study to compare changes over time in the prevalence of NSAID use and rates of admission to hospital because of upper GI bleeding after the introduction of COX-2 inhibitors in the elderly populations of British Columbia and Ontario. (
  • COX-2 is considered an inducible isoenzyme, induced by pain and inflammatory stimuli. (
  • To examine selectivity of tolerated doses of an inhibitor of the inducible COX-2 in humans, we examined the effects of celecoxib on indices of COX-1-dependent platelet thromboxane (Tx) A 2 and on systemic biosynthesis of prostacyclin in vivo . (
  • Indomethacin is a nonselective COX1 and COX2 inhibitor with IC50 of 0.1 μg/mL and 5 μg/mL, respectively, used to reduce fever, pain, stiffness, and swelling. (
  • Volunteers received doses of 100, 400, or 800 mg of celecoxib or 800 mg of a nonselective inhibitor, ibuprofen. (
  • Selective COX-2 inhibitors (COXIBs) have been shown to possess much improved GI tolerability and reduced GI related adverse events when compared with nonselective COX-1inhibitors. (
  • Diclofenac is a potent and nonselective anti-inflammatory agent, acts as a COX inhibitor, with IC50s of 4 nM, 1.3 nM for human COX-1 and COX-2 in CHO cells, and 5.1, 0.84 μM for ovine COX-1 and COX-2, respectively. (
  • Also called cyclo-oxygenase-2 inhibitor. (
  • 1 - 3 The introduction of new anti-inflammatory agents, with more specific inhibitory effects on cyclo-oxygenase 2 (COX 2) pathways, promised equivalent efficacy with greater safety and tolerability. (
  • This review summarizes our current understanding of the role of cyclo-oxygenase inhibitors (COXI) in influencing the structural development as well as the function of the developing kidney. (
  • Cyclo-oxygenase (COX) inhibitors inhibit uterine contractions, are easily administered and appear to have few maternal side effects. (
  • Evidence of enhanced gastrointestinal safety with any of the new cyclo-oxygenase-2 inhibitors compared with non-selective non-steroidal anti-inflammatory drugs is lacking, say the authors. (
  • The benefit of cyclo-oxygenase-2 (COX-2) inhibitors in preventing serious gastrointestinal adverse events is likely overstated. (
  • 2006) Risk of upper gastrointestinal ulcer bleeding associated with selective cyclo-oxygenase-2 inhibitors, traditional non-aspirin non-steroidal anti-inflammatory drugs, aspirin and combinations. (
  • Jones, P. and Lamdin, R. (2010) Oral Cyclo-Oxygenase 2 Inhibitors versus Other Oral Analgesics for Acute Soft Tissue Injury Systematic Review and Meta-Analysis. (
  • Selective cyclooxygenase-2 (COX-2) inhibitors have provided relief for patients suffering from chronic pain and other inflammatory conditions and have reduced adverse gastrointestinal effects. (
  • Disclosed is a pharmaceutical composition including a therapeutic quantity of a COX-2 inhibitor having an IC50-WHMA COX-2/COX-1 ratio ranging from about 0.23 to about 3.33 with reduced gastrointestinal and cardiovascular toxicity. (
  • Increased risks of adverse gastrointestinal events were associated with current use of COX-2 inhibitors and with conventional non-steroidal anti-inflammatory drugs. (
  • Population rates of upper gastrointestinal (GI) hemorrhage have been observed to increase with the introduction and rapid uptake of selective cyclooxygenase-2 (COX-2) inhibitors. (
  • Dr. A Mark Fendrick, professor of internal medicine and health management and policy at the University of Michigan, believes that this study illuminates the increased dangers of gastrointestinal (GI) bleeding when a COX-2 inhibitor and aspirin are used together. (
  • However, the use of the COX-2 inhibitors and the associated excess cardiovascular risk has caused increasing concern since the publication of the Vioxx Gastrointestinal Outcomes Research (VIGOR) study 1 in 2000. (
  • Inhibiting both COX-1 and -2 simultaneously can have side effects such as gastrointestinal bleeding and renal dysfunction. (
  • 1 The literature suggests that the principal 'advantage' of upper gastrointestinal safety is lost when a COX-2 inhibitor is co-prescribed with aspirin. (
  • ATLANTA-Parecoxib, the first injectable COX-2 inhibitor, demonstrated impressive analgesic efficacy in postsurgical patients, according to a study presented at the 19th Annual Scientific Meeting of the American Pain Society (APS). (
  • Dr. Blanke said that COX-2 inhibitors enhance the efficacy of radiotherapy in mouse sarcomas. (
  • Early studies have also found that COX-2 inhibitors can increase the efficacy of cytotoxic drugs. (
  • The purpose of this research project was to determine the efficacy of the cyclooxygenase (COX) and lipoxygenase (LOX) inhibitors, alone or in combination, to prevent OH-BBN-induced urinary bladder cancers in female Fischer-344 rats. (
  • In conjunction with the recent development of next generation, highly selective COX-2 inhibitors, they can be expected to lead to even greater efficacy of their use as adjuncts to various anticancer agents for the treatment of high-risk patients without compromising their quality of life. (
  • Efficacy Assessment of Meloxicam, a Preferential Cyclooxygenase-2 Inhibitor, in Acute Coronary Syndromes Without ST-Segment Elevation. (
  • Structure activity relationship (SAR) studies for diaryl heterocyclic compounds have indicated that a cis-stilbene moiety and changes in the para-position of one of the aryl rings play an important role in COX-2 selectivity. (
  • 2. The method of claim 1 wherein the cyclooxgenase-2 selective inhibitor has a selectivity ratio of COX-1 IC 50 to COX-2 IC 50 not less than about 50. (
  • Both 15 and 16 showed high selectivity and affinity toward COX-2 isozyme over COX-1, which is in agreement with the experimental results. (
  • Six compounds had potencies in the submicromolar range against COX-2 and higher selectivity for COX-2 vs. COX-1 compared to the currently used drug celecoxib. (
  • Disclosed is an extended release pharmaceutical formulation comprising a muscle relaxant drug, such as tizanidine, in combination with a cyclooxygenase-2 inhibitor, such as valdecoxib. (
  • Cyclooxygenases are enzymes that take part in a complex biosynthetic cascade that results in the conversion of polyunsaturated fatty acids to prostaglandins and thromboxane(s). (
  • Prostaglandins and thromboxane are formed by the enzymatic oxidation of arachidonic acid catalyzed by the cyclooxygenases, COX 1 and COX-2. (
  • Cyclooxygenase (COX) enzymes play an important role in the synthesis of prostaglandins. (
  • The cyclooxygenases are required for the creation of prostaglandins. (
  • COX-1 and COX-2 enzymes act upon arachadonic acid to form molecules called prostaglandins. (
  • From a clinical perspective, one of the enzymes that are involved in the production of the destructive prostaglandins, called cyclooxygenase-2 (COX-2), is the target of nutritional intervention in order to suppress these substances. (
  • Phloretin inhibits phorbol ester-induced tumor promotion and expression of cyclooxygenase-2 in mouse skin. (
  • Primarily inhibits COX-2. (
  • Some studies have demonstrated that gestational age, birth weight, B-type natriuretic peptide (BNP), and ductal diameter can predict the therapeutic responsiveness to COX inhibitors. (
  • This invention relates to therapeutic compositions that exhibit anti-inflammatory properties and inhibit cyclooxygenase. (
  • At therapeutic doses, they do not affect COX-1, which helps regulate normal cell function in the stomach and blood. (
  • Cyclooxygenase-2 (COX-2) is overexpressed in DCIS, representing another potential therapeutic target. (
  • Cycloxygenase-2 is expressed in DCIS but the cycloxygenase-2 inhibitor celecoxib had no effect on either proliferation or apoptosis and is unlikely to have therapeutic value in DCIS. (
  • These results suggest that selective cyclooxygenase-2 inhibitors may be a valuable therapeutic strategy for ischemic brain injury. (
  • Neuroprotection afforded by nimesulide is observed even when the treatment is delayed until 6 h after the onset of ischemia, confirming a wide therapeutic window of COX-2 inhibitors in experimental stroke. (
  • COX-2 inhibitors have analgesic and anti-inflammatory activity by blocking the transformation of arachidonic acid into prostaglandin H2 selectively. (
  • Together, PGs comprise a diverse family of biologically active lipids derived from the enzymatic conversion of arachidonic acid by COX to PGG 2 /H 2 followed by the generation of five primary bioactive prostanoids PGE 2 , PGI 2 , PGD 2 , PGF 2α and thromboxane A 2 [ 4 , 5 , 6 ]. (
  • COX enzymes metabolize arachidonic acid, forming prostaglandin H2, which is subsequently metabolized by prostaglandin E synthase into prostaglandin E2 (PGE2) [ 9 , 10 ]. (
  • They are formed from arachidonic acid by the catalytic activity of prostaglandin G/H synthase, also known colloquially as cyclooxygenase (COX) ( 2 ). (
  • Cyclooxygenase-1 (Cox-1) and cyclooxygenase-2 (Cox-2) are prostaglandin synthases that catalyze the formation of PGH 2 from arachidonic acid (AA). (
  • Whole embryo culture was used in which day-9 embryos were exposed to high concentrations of glucose, arachidonic acid, prostaglandin (PG)E2, COX inhibitors, and antioxidants for 48 h. (
  • Supplementation of either arachidonic acid or PGE2 to the culture medium with COX inhibitors in low glucose rectified the embryonic development, and PGE2 supplementation also normalized the development of embryos cultured with COX inhibitors in high glucose concentration. (
  • These results add strength to the hypothesis that arachidonic acid metabolism inhibitors are an effective class of agents against bladder cancer. (
  • 16] L.J. Marnett, S.W. Rowlinson, D.C. Goodwin, A.S. Kalgutkar, C.A. Lanzo, Arachidonic acid oxygenation by COX-1 and COX-2. (
  • Nimesulide, a cyclooxygenase-2 (COX-2) inhibitor, delays the progression of precancerous pancreatic lesions in mice, according to researchers at David Geffen School of Medicine at UCLA. (
  • In the future, Dr. Eibl and others plan to study the long-term effects of nimesulide and additional COX-2 inhibitors on the onset and progression of pancreatic cancer. (
  • In vitro studies of NSCLC cells treated with irinotecan (Camptosar), docetaxel (Taxotere), etoposide (VePesid), or cisplatin (Platinol), with or without the COX-2 inhibitor nimesulide showed that the COX-2 inhibitor alone induced apoptosis at low concentrations and was 'near-synergistic' for selected anticancer agents, according to Dr. Blanke. (
  • Our study shows that a cyclooxygenase (COX)-2 inhibitor, nimesulide, can inhibit proliferation of non-small cell lung cancer cell lines in vitro in a dose-dependent manner, in part by inducing apoptosis even at clinically achievable low concentrations. (
  • In this study, we examined whether nimesulide can inhibit the proliferation of NSCLC cells and whether sensitivity to nimesulide is related to COX-2 expression levels and the p53 gene status. (
  • We injected colon 26, a colorectal cancer cell line, in CDF1 mouse spleen and, from the following day, two kinds of COX-2 inhibitor (etodolac and nimesulide) were administered orally. (
  • The expression of COX-2 mRNA was also significantly lower in the etodolac-treated group than in controls (p=0.04), but not in the nimesulide-treated group. (
  • GW406381, a highly selective cyclooxygenase-2 (COX-2) inhibitor, attenuates spontaneous ectopic discharge in sural nerves of rats following chronic constriction injury. (
  • In this study we examined whether the highly selective cyclooxygenase-2 inhibitor DFU reduces neuronal damage when administered several hours after 5 min of transient forebrain ischemia in gerbils. (
  • Mitomycin-C (Mutamycin) induces COX-2 in MKN-74 gastric cancer cells, and this induction causes cellular resistance to apoptosis. (
  • Paired baseline and end point biopsies were analyzed for proliferation (Ki67), apoptosis, human epidermal growth factor receptor 2 (HER2), COX-2, and progesterone receptor (PR) expression by immunohistochemistry. (
  • Researchers were surprised at the results because Drosophila do not have COX-2 enzymes. (
  • Cyclooxygenase enzymes play a vital role in inflammatory pathways in the human body. (
  • Some anti-inflammatory drugs act by inhibiting both cyclooxygenase-2 (COX-2) and COX-1 enzymes. (
  • COX-1 enzymes are produced widely throughout the body and is involved in the regulation of day-to-day cellular and metabolic activities such as maintaining stomach lining integrity, regulating blood flow within the kidneys and balancing platelet function. (
  • COX-1 enzymes are present in the body always and should not be inhibited. (
  • COX-2 enzymes are necessary for inducing pain. (
  • The consumption of high amounts of saturated fat and the omega 6 unsaturated fatty acids, and a consumption of low amounts of omega 3 fatty acids can give rise to the production of COX-2 enzymes. (
  • It's not that COX-2 enzymes are 'bad' enzymes. (
  • It's just that our diets and the stresses we live in today create way too much COX-2 enzymes, and we don't use the resources to put out the fires. (
  • Celecoxib and other COX-2 selective inhibitors, valdecoxib, parecoxib, and mavacoxib, were discovered by a team at the Searle division of Monsanto led by John Talley. (
  • At this stage, there is insufficient information available to comment on the cardiovascular safety of the other COX-2 inhibitors (i.e. celecoxib, etoricoxib, meloxicam, parecoxib and valdecoxib). (
  • COX-2 plays a major role in prostaglandin biosynthesis in inflammatory cells and in the central nervous system. (
  • and ( iii ) COX-2 is a major source of systemic prostacyclin biosynthesis in healthy humans. (
  • Of note, the simultaneous addition of SC-236 and CJ-13,610 resulted in a higher inhibitory profile on PGE2 biosynthesis than the dual COX/5-LO inhibitor licofelone. (
  • Although their actions are largely thought to be mediated by the blockade of prostaglandin (PG) biosynthesis, evidences suggesting endogenous opioid peptide link in spinal antinociception of COX inhibitor have been reported. (
  • Accordingly, selective inhibitors of cyclooxygenase (COX)-2 are one of the most widely used analgesics and its actions are well established to be mediated by the blockade of prostaglandin biosynthesis. (
  • Given the risks, several management strategies have been developed to induce closure of the PDA, including treatment with the COX inhibitors indomethacin and ibuprofen. (
  • Cyclooxygenase (COX) inhibitors, such as indomethacin and ibuprofen, are often used for the treatment of PDA in preterm infants, and they work by reducing the production of prostaglandin. (
  • What is the role of cyclooxygenase (COX) inhibitors in the treatment of dysmenorrhea? (
  • Sinicrope FA, Gill S. Role of cyclooxygenase-2 in colorectal cancer. (
  • Prevention of hydroxybutyl(butyl)nitrosamine(OH-BBN)-induced urinary bladder cancer in Fischer-344 rats by cyclooxygenase and lipoxygenase inhibitors. (
  • 17] T. Nakagomi, T. Sasaki, T. Kirino, A. Tamura, M. Noguchi, I. Saito, K. Takakura, Effect of cyclooxygenase and lipoxygenase inhibitors on delayed neuronal death in the gerbil hippocampus, Stroke 20 (1989) 925-929. (
  • COX-2 inhibitors are used in the treatment of arthritis and acute gout. (
  • They included older people and patients with chronic kidney disease or rheumatoid arthritis who started treatment with COX-2 inhibitors. (
  • The novel cyclooxygenase- (COX)-2 inhibitor celecoxib is an effective treatment for the signs and symptoms of osteoarthritis and rheumatoid arthritis. (
  • The regulator's remarks come close on the heels of comments by a U.S. advisory panel on Friday that Merck & Co Inc.'s withdrawn COX-2 inhibitor arthritis drug, Vioxx, was safe enough to rejoin Pfizer's rival pain relievers, Celebrex and Bextra, on the U.S. market. (
  • As an example, at the time of writing, a perusal of the South Africa n MIM S (September 2010) indicated that there are three locally available specific cyclooxygenase-2 inhibitors (COXIBs) namely, celecoxib, etoricoxib (indicated for the treatment of rheumatoid arthritis and osteoarthritis) and parecoxib (indicated for the treatment postoperative pain) that all contain a sulfonamide substituent. (
  • The researchers were able to achieve similar heart-stopping results in rat cardiac cells, whereas aspirin, another potent COX-2 inhibitor, had no effect, confirming that another mechanism is at work. (
  • A new report in the December 3 issue of the British Medical Journal finds that COX-2 inhibitors are just as harmful to the stomach as traditional anti-inflammatory medications like aspirin. (
  • It is fine to take a cox-2 inhibitor for joint pain and an aspirin for your heart, but "when you combine these two, they really present GI problems. (
  • Aspirin and caffeic acid, (COX and LOX inhibitors, respectively) were also modestly effective and noneffective respectively in inhibiting urinary bladder cancer. (
  • Dr. Blanke said that COX-2 is expressed in human colorectal cancer neovasculature, including liver metastases, and that expression in the neovasculature is actually greater than in the tumor cells. (
  • COX-2 expression is also associated with risk of colorectal cancer recurrence. (
  • F344 rats were treated with COX-1 inhibitors (SC560), COX-2 inhibitors (indomethacin, etodolac, or celecoxib), a β-blocker (propranolol), or a combination of a COX-2 inhibitor and a β-blocker (etodolac and propranolol). (
  • These findings indicate that the selective COX-2 inhibitor, etodolac, suppresses liver metastasis by reducing MMP-9 activity. (
  • See 'COX-2 selective inhibitors: Adverse cardiovascular effects' . (
  • Reviewing the clinical evidence, particularly the complex cardiovascular effects of the COX inhibitors, the article discusses the clinical relevance of their thrombogenic and anti-atherosclerotic potential. (
  • Since many of the studies are retrospective analyses, randomised clinical trials are needed to ascertain whether these cardiovascular effects constitute a problem or an unexpected benefit, and whether there are differences between the different COX-2 inhibitors. (
  • COX-2 inhibitors also have been shown to cause adverse cardiovascular effects when administered at high doses over long durations. (
  • Our recent study indicated that celecoxib (SC-58635), a specific COX-2 inhibitor, suppressed colonic aberrant crypt foci formation induced by azoxymethane in rats and led us to investigate more specifically the chemopreventive potential of this compound using colon tumors as end points. (
  • The results of this study provide evidence, for the first time, that a specific COX-2 inhibitor, celecoxib, possesses strong chemopreventive activity against colon carcinogenesis. (
  • The non-steroidal anti-inflammatory drug, sulindac and a specific COX-2 inhibitor, NS398, were shown to act similarly in LPS-activated RAW 264.7 cells. (
  • Cyclooxygenases have two main isoforms that are called COX-1 and COX-2 (as well as a COX-3). (
  • volume of conference proceedings reviews the general pathophysiological significance of the isoforms of cyclooxygenase, and the likely value of selective COX-2 inhibitors in the treatment of rheumatoid conditions. (
  • COX-2 inhibitors are important drugs with analgesic and anti-inflammatory effects. (
  • The team looked at information on these patients' history of COX-2 inhibitor use, including when they were using these drugs and what type of COX-2 inhibitors they were taking. (
  • We studied the effect of celecoxib, a selective cyclooxygenase-2 inhibitor, on colorectal polyps in patients with familial adenomatous polyposis. (
  • In patients with familial adenomatous polyposis, six months of twice-daily treatment with 400 mg of celecoxib, a cyclooxygenase-2 inhibitor, leads to a significant reduction in the number of colorectal polyps. (
  • The study, published in the August 1 issue of Cancer Research, a journal of the American Association for Cancer Research, suggests a potential role for COX-2 inhibitors in pancreatic cancer prevention among high-risk patients. (
  • Methods: After approval by the institutional ethics and a scientific committee, and obtaining informed consent , patients admitted to the emergency department (ED) due to blunt trauma with a diagnosis of lung contusion will be enrolled in the study.The effects of statins and COX 2 inhibitors on ALI will be assessed by recording clinical parameters and measuring inflammatory mediators levels in the serum and in the bronchoalveolar space. (
  • In patients with previous peptic ulcer, is celecoxib (Celebrex) safer than naproxen taken with an proton pump inhibitor? (
  • PORTLAND, Oregon-Cyclooxygenase 2 (COX-2) inhibitors are attracting attention as potential anti-cancer drugs because of evidence of increased survival in patients with low levels of COX-2. (
  • Dr. Blanke said that COX-2 overexpression is significantly correlated with metastases, and particularly with hematogenous metastasis in patients with resected large bowel malignancies. (
  • Patients at risk of CV disease or with a history of CV disease were the most significant determinants of CV events after receiving COX inhibitors. (
  • The results of this study suggest the need for careful monitoring and control of blood pressure when COX-2-specific inhibitors and nonspecific nonsteroidal anti-inflammatory drugs are prescribed to patients with hypertension and type-2 diabetes, said Dr. White. (
  • Doctors must be on the lookout for potential kidney side effects when they prescribe COX-2 inhibitors, particularly in older patients. (
  • Because natriuretic peptide levels reflect intravascular volume and pressure, it is hypothesized that when patients are prescribed medications that promote fluid retention-such as non-selective nonsteroidal anti-inflammatory drugs and cyclooxygenase-2 inhibitors-monitoring natriuretic peptide levels before and after initiating the medication may allow these medications to be used more safely. (
  • COX-2 inhibitors have been found to be effective in suppressing inflammatory neurodegenerative pathways in mental illness, with beneficial results in trials for major depressive disorder as well as schizophrenia . (
  • There is no evidence to back up claims that the new generation of anti-inflammatory drugs (COX-2 inhibitors) are less harmful to the stomach lining than many traditional anti-inflammatory drugs, concludes a study in this week s BMJ. (
  • however, the upregulation of pro-inflammatory COX-2 and increased production of COX-2 derived metabolites have been implicated in diabetic nephropathy. (
  • These observations have led to the hypothesis that COX-2 expression mediates the enhanced prostanoid release, which characterizes the inflammatory response ( 21 ). (
  • Chamomile, a novel and selective COX-2 inhibitor with anti-inflammatory activity. (
  • Serrapeptase is also a natural COX-2 inhibitor, a natural pain killer, parts of Asia and Europe have been using Serrapeptase instead of the traditional steroidal anti-inflammatory drugs prescribed now a days. (
  • Francis P, Chakraborty K. An anti-inflammatory salmachroman from the sea urchin Salmacis bicolor: a prospective duel inhibitor of cyclooxygenase-2 and 5-lipoxygenase. (
  • This explains the efforts to obtain drugs able to inhibit both 5-lipoxygenase and cyclooxygenases: the so-called dual acting anti-inflammatory drugs. (
  • Intrathecal DUP-697, a selective COX-2 inhibitor, effectively relieved inflammatory pain in rats. (
  • Thus, µ, δ and κ opioid receptor antagonists were intrathecally administered to investigate the ability of opioid receptor subtype antagonists to reverse the antinociception induced by COX-2 inhibitor in the formalin test which shows an early phase of acute nociceptive response followed by a late phase response being related to more complex inflammatory reactions. (
  • Can Natriuretic Peptide Levels Predict the Cardiovascular Complications of COX-2 Inhibitors and Nonsteroidal Anti-inflammatory Drugs? (
  • Purpose The purpose of this study is to evaluate the effect of two anti-inflammatory drugs, fish oil capsules and the COX-2 inhibitor celecoxib, on pregnancy associated breast cancer (PABC). (
  • The study shows that people who were current users of COX-2 inhibitors were 19% more likely to die after a stroke than people who did not use COX-2 inhibitors. (
  • The local pattern of use indicated that users of COX-2 inhibitors were older, had other co-morbidities and were often on multiple medicines that could have increased their risk of this type of event. (
  • These results suggest that COX-2 inhibitors may not be as safe as originally thought, although a possible confounding effect cannot be ruled out, they conclude. (
  • However, some studies in animals suggest that COX-2 inhibitors also can cause kidney problems. (
  • sulfones and sulfonamides are selective for COX-2 but sulfoxides and sulfides are not. (
  • The professional information leaflets of three locally available specific cyclooxygenase-2 inhibitors indicate that these drugs are contraindicated in persons with a known allergy to sulfonamides. (
  • Similarly, COX-2 mRNA is increased in 86% of CRC and in over 40% of colorectal polyps. (
  • In addition, chamomile caused reduction in LPS-induced COX-2 mRNA and protein expression, without affecting COX-1 expression. (
  • TP significantly suppressed the production of NO production, blocked the mRNA expression of iNOS, and COX-2 in both cell lines, blocked the mRNA expression of TNF-α, IL-1β, IL-6, and PGE 2 in the murine cell line. (
  • In addition, COX-2 mRNA, matrix metalloproteinase (MMP)-9 mRNA, and tissue inhibitor of MMP (TIMP)-1 mRNA of cancer tissue were measured by means of real-time RT-PCR. (
  • Expression of COX-2 mRNA and MMP-9 mRNA correlated significantly (r=0.78, p=0.001), but there was no correlation between either COX-2 mRNA and TIMP-1 mRNA expression or between MMP-9 mRNA and TIMP-1 mRNA expression. (
  • 13] J. Koistinaho, S. Koponen, P.H. Chan, Expression of cyclooxygenase-2 mRNA after global ischemia is regulated by AMPA receptors and glucocorticoids, Stroke 30 (1999) 1900-1906. (
  • The effectiveness of sunitinib for the treatment of renal cell carcinoma could be enhanced with the addition of a cyclooxygenase-2 inhibitor, study findings show. (
  • COX-2 regulation and its association with renal damage are not known in the Obese Zucker rat. (
  • Protein expression of COX-1 and COX-2 in the kidney cortex, renal microvessels and glomeruli was studied. (
  • After several COX-2 inhibiting drugs were approved for marketing, data from clinical trials revealed that COX-2 inhibitors caused a significant increase in heart attacks and strokes, with some drugs in the class having worse risks than others. (
  • However, he stressed to heart wire , "a mouse study is not reason enough for people to stop taking COX-2 inhibitors," and that much more clinical work would be required to determine whether the murine data can be extrapolated into humans. (
  • However, as observed in clinical practice, not all PDAs in preterm infants can be closed using COX inhibitors. (
  • Patient race is a significant predictor of COX-2 prescriptions in the Medicaid population, even after adjusting for other demographic and clinical variables. (
  • Another expert, Dr. Eric Matteson, a professor of medicine at the Mayo Clinic College of Medicine in Rochester, Minnesota, believes the study reveals COX-2 inhibitors increase the risk of GI bleeding and ulcers when used in clinical practice. (
  • The typical use of COX-2 agents in practice is for shorter duration, and at lower doses, than was employed in randomized clinical trials. (
  • Because our previous studies have indicated a significantly increased COX-2 expression in up to 70% of adenocarcinoma cases, the present findings are of great clinical interest. (
  • In the March 1 issue of Clinical Cancer Research, researchers from University of Wisconsin-Madison demonstrate that low doses of the COX-2 inhibitor celecoxib, administered with a green tea polyphenol called pigallocatechin-3-gallate (EGCG), can slow the growth of human prostate cancer. (
  • COX-2 inhibitors are being studied in the prevention of colon polyps, and as anticancer drugs. (
  • While newer versions of these COX-2 inhibitor drugs have been pulled off shelves, older ones are still frequently prescribed. (
  • Earlier this year, scientists from the Perelman School of Medicine at the University of Pennsylvania, PA, published a report in the Proceedings of the National Academy of Sciences of research into a potential new class of drugs that could provide a safer alternative to COX-2 inhibitors . (
  • They also stress it is too early to speculate on human effects, although their results suggest Drosophilaâ€"one of the most valuable of organisms in biological research and has been used as a model research organism for almost a centuryâ€"are a valuable tool to investigate other COX-2 drugs. (
  • This includes the COX-2 drugs. (
  • Of course, if this is so, all of the hype and expense associated with the COX-2s was for naught and the only ones that benefited from the drugs were (and are) Merck and Pfizer, which have made tens of billions of dollars in profits from Vioxx, Celebrex, and Bextra. (
  • In recent years, several additional intracellular components (besides COX-2) were discovered that appear to be important for mediating the anticancer effects of celecoxib in the absence of COX-2. (
  • Additional support for the idea that other targets besides COX-2 are important for celecoxib's anticancer effects has come from studies with chemically modified versions of celecoxib. (
  • Last year, Medical News Today also reported on a study that suggested a possible "fix" for the side effects associated with COX-2 inhibitors. (
  • COX inhibitors may have adverse effects on the baby's heart, lungs and kidneys, and on the mother. (
  • However, adverse effects have been reported in the fetus and newborn as a result of exposure to COX inhibitors. (
  • To assess the effects on maternal and neonatal outcomes of COX inhibitors administered as a tocolytic agent to women in preterm labour when compared with (i) placebo or no intervention and (ii) other tocolytics. (
  • In addition, to compare the effects of non-selective COX inhibitors with COX-2 selective inhibitors. (
  • To study the effects of COX-2 on PanIN progression, Dr. Eibl and colleagues focused on the KrasG12D mouse, an animal model that mimics the early stages of pancreatic cancer. (
  • Aims: The current study aims at evaluating the beneficial effects of statins and COX-2 receptor inhibitors on ALI elicited by blunt trauma to the chest. (
  • Singh and colleagues point out that since these arrhythmia effects bypass COX-2, it is unclear if other COX-2 inhibitors would yield similar results. (
  • Molecular docking result indicated that the inhibitory effects of TP on COX-2 and PGE 2 could be attributed to acteoside, which is the main compound of TP that could bind to the catalytic zone of COX-2. (
  • Pre-treatment with naltrexone diminished the analgesic effects of a COX-2 inhibitor, and its antinociception was abolished in rats made tolerant to the analgesic effects of morphine [ 4 ]. (