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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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);
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.
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.
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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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 ...
Several COX-2 inhibitors, such as rofecoxib (Vioxx), have been withdrawn from the market, after evidence emerged that PTGS2 ... COX-1 and COX-2, are acted on by aspirin. Aspirin irreversibly inhibits COX-1 and modifies the enzymatic activity of COX-2. COX ... "Cyclooxygenase-3 (COX-3): filling in the gaps toward a COX continuum?". Proceedings of the National Academy of Sciences of the ... Several trials suggest that the simultaneous use of a COX-2 inhibitor with aspirin may increase the risk of gastrointestinal ...
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 ...
It is a COX-1 inhibitor. It also inhibits the activation of nuclear factor k-B, which in turn regulates the expression of the ... Triflusal is a platelet aggregation inhibitor that was discovered and developed in the Uriach Laboratories, and commercialised ... Triflusal is a selective platelet antiaggregant through; blocks cyclooxygenase, thereby inhibiting thromboxane A2, and thus ...
... 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. ... Gross GJ, Moore J (July 2004). "Effect of COX-1/COX-2 inhibition versus selective COX-2 inhibition on coronary vasodilator ... Naproxen is a nonselective COX inhibitor. As an NSAID, naproxen appears to exert its anti-inflammatory action by reducing the ... 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 ...
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. The most popular drug of the oxicam class is ...
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 ...
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 ... COX-2 inhibitors, Nonsteroidal anti-inflammatory drugs, Fluoroarenes, Sulfonamides, Pyrazoles, Trifluoromethyl compounds, All ... 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 ... COX-2 inhibitors, Nonsteroidal anti-inflammatory drugs, Imidazoles, Fluoroarenes, Organochlorides, Sulfonamides, All stub ... Activity Relationship of a New Series of COX-2 Selective Inhibitors: 1,5-Diarylimidazoles". Journal of Medicinal Chemistry. 46 ...
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 is a COX-2 inhibitor (coxib). Gaynor JS, Muir WM (2014). "Robenacoxib". Handbook of Veterinary Pain Management (3rd, revised ... COX-2 inhibitors, Nonsteroidal anti-inflammatory drugs, Fluoroarenes, Anilines, Carboxylic acids, Veterinary drugs, All stub ...
... 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. ...
Multiple cyclooxygenase inhibitors are already used as drugs against thrombotic diseases. These drugs inhibit both the ... Furegrelate is an enzyme inhibitor. It combines with the enzyme thromboxane A2 synthase to prevent the normal substrate-enzyme ... In platelets this fatty acid is metabolized to an endoperoxide called prostaglandin H2 by the enzyme cyclooxygenase 1. This ... Johnson RA, Nidy EG, Aiken JW, Crittenden NJ, Gorman RR (August 1986). "Thromboxane A2 synthase inhibitors. 5-(3-Pyridylmethyl) ...
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 (the COX-1 and COX-2 isoenzymes). In cells, these enzymes are ...
COX inhibitors that are relatively selective for the COX-1 enzyme, such as ketoprofen and flurbiprofen. Conversely, COX ... The majority work by inhibiting the activity of the cyclooxygenase (COX) family of enzymes in the body. Nonselective COX enzyme ... These are also primarily nonselective COX inhibitors, but also work through other mechanisms including activating AMP-activated ... Cryer B, Feldman M (May 1998). "Cyclooxygenase-1 and cyclooxygenase-2 selectivity of widely used nonsteroidal anti-inflammatory ...
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 ( ...
Immunosuppressant drugs such as corticosteroids, cyclooxygenase inhibitors, interferon alpha may be effective. A 2020 review ...
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, along with other COX-2 selective inhibitors, celecoxib, valdecoxib, and mavacoxib, were discovered by a team at the ... Parecoxib is the first parenteral COX-2 selective inhibitor available for clinical use in pain management. Its first ...
Aspirin and other cyclooxygenase inhibitors can significantly prolong bleeding time. While warfarin and heparin have their ...
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- ...
Arachidonic acid Cyclooxygenase Cyclooxygenase 1 NSAID Discovery and development of COX-2 selective inhibitors COX-2 selective ... "Inducible COX-2 dominates over COX-1 in prostacyclin biosynthesis: Mechanisms of COX-2 inhibitor risk to heart disease". Life ... Non-substrate FAs can potentiate or attenuate PTGS (COX) inhibitors depending on the fatty acid and whether the inhibitor binds ... COX) inhibitors. PTGS2 (COX-2) is unexpressed under normal conditions in most cells, but elevated levels are found during ...
Nelson DL, Cox MM (2005). Lehninger Principles of Biochemistry. New York: W. H. Freeman and company. p. 841. ISBN 978-0-7167- ... The enzymes that catalyze these chemical reactions can then be purified and their kinetics and responses to inhibitors ... ISBN 0-7167-4955-6. Cox M, Nelson DL (2004). Lehninger Principles of Biochemistry. Palgrave Macmillan. ISBN 0-7167-4339-6. ...
... bifunctional inhibitor proteins from plant seeds and various serine proteases and their inhibitors have been determined by his ... cyclooxygenase, lipoxygenase, endothelin receptor, endothelin converting enzyme, breast cancer regression proteins and matrix ... These design rules are being exploited for making specific peptides to act as tight inhibitors of target enzymes and potent ... "Structures and binding studies of the complexes of phospholipase A2 with five inhibitors". Biochimica et Biophysica Acta (BBA ...
Schipper, J.; Chanson, J. S.; Chiozza, F.; Cox, N. A.; Hoffmann, M.; Katariya, V.; Lamoreux, J.; Rodrigues, A. S. L.; Stuart, S ... There is also controversy over the use of muzzles and other inhibitors, which prevent the dolphins from foraging for food while ...
Inhibitors of CYP2B6 can be classified by their potency, such as: Strong inhibitor being one that causes at least a 5-fold ... Obach RS, Cox LM, Tremaine LM (February 2005). "Sertraline is metabolized by multiple cytochrome P450 enzymes, monoamine ... Weak inhibitor being one that causes at least a 1.25-fold but less than 2-fold increase in the plasma AUC values, or 20-50% ... Moderate inhibitor being one that causes at least a 2-fold increase in the plasma AUC values, or 50-80% decrease in clearance. ...
"Endogenous N-acyl-dopamines induce COX-2 expression in brain endothelial cells by stabilizing mRNA through a p38 dependent ... cannabinoid-receptor ligands and inhibitors of anandamide inactivation with cannabimimetic activity in vitro and in vivo". The ...
In cells, COX-1 and COX-2 metabolize arachidonic acid to PGH2 which is then converted to PGE2 by any one of three isozymes, ... "Anti-inflammatory cyclopentenone prostaglandins are direct inhibitors of IkappaB kinase". Nature. 403 (6765): 103-8. Bibcode: ... the COX's also metabolizes dihomo-gamma-linolenic acid to PGH1 which is metabolized by one of the three PTGES isomzymes to PGE1 ...
showed that such high concentrations of D-2HG could act as a direct inhibitor of lactate dehydrogenase in mouse T cells. ... ISBN 0-9747077-1-6. Cox M, Nelson DR, Lehninger AL (2005). Lehninger Principles of Biochemistry. San Francisco: W.H. Freeman. ... "Clinical development of IDH1 inhibitors for cancer therapy". Cancer Treatment Reviews. 103: 102334. doi:10.1016/j.ctrv. ...
Calcineurin inhibitors (such as pimecrolimus, tacrolimus or cyclosporin) are sometimes used. While topical steroids are widely ... Li TJ, Cui J (August 2013). "COX-2, MMP-7 expression in oral lichen planus and oral squamous cell carcinoma". Asian Pacific ...
For instance, aspirin is a widely used drug that acts as a suicide inhibitor of the cyclooxygenase enzyme. This inhibition in ... reverse-transcriptase inhibitors targeting HIV/AIDS, neuraminidase inhibitors targeting influenza, and terminase inhibitors ... For example, an inhibitor might compete with substrate A for the first binding site, but be a non-competitive inhibitor with ... New inhibitors are used to obtain crystallographic structures of the enzyme in an inhibitor/enzyme complex to show how the ...
MS can thus be considered a dual inhibitor of 5-LOX and COX pathways of arachidonic acid cascade. Further investigation with ... Also in trials for CRPC are : checkpoint inhibitor ipilimumab, CYP17 inhibitor galeterone (TOK-001), and immunotherapy PROSTVAC ... While the commonly used inhibitors produced strong cytotoxicity, notably, zileuton, the only commercialized 5-LOX inhibitor, ... X-linked inhibitor of apoptosis (XIAP) is hypothesized to promote cancer cell survival and growth, the Macrophage inhibitory ...
Xu W, Cox CS, Li Y (2011). "Induced pluripotent stem cells for peripheral nerve regeneration". Journal of Stem Cells. 6 (1): 39 ... A 2007 Cochrane review of aldose reductase inhibitors for the treatment of the pain deriving from diabetic polyneuropathy found ... Chalk C, Benstead TJ, Moore F (October 2007). "Aldose reductase inhibitors for the treatment of diabetic polyneuropathy". The ... imapramine, and desipramine,) serotonin-norepinephrine reuptake inhibitor (SNRI) medications (duloxetine, venlafaxine, and ...
Table 1: Endogenous opioid peptides {{cite journal}}: External link in ,quote= (help) Toll L, Caló G, Cox BM, Chavkin C, ... Opiorphin and spinorphin, enkephalinase inhibitors (i.e., prevent the metabolism of enkephalins). Hemorphins, hemoglobin- ...
... and Cyclo-oxygenase 2 (COX2) genes. Genetic data from over 7,600 cancer patients shows that over 1% has the deactivated CUX1 ... the Wellcome Trust Sanger Institute reported that the mutation of CUX1 reduces the inhibitory effects of a biological inhibitor ...
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. Cyanotoxins are often implicated in what are commonly called red tides or ... Cox PA, Davis DA, Mash DC, Metcalf JS, Banack SA (2015). "Dietary exposure to an environmental toxin triggers neurofibrillary ...
The ADD domain serves as an inhibitor of the methyltransferase domain until DNMT3A binds to the unmodified lysine 4 of histone ... Cox T, Jackson D, Severin J, Biggs P, Fu J, Nefedov M, de Jong PJ, Stewart AF, Bradley A (June 2011). "A conditional knockout ...
"Evaluation of COX-1/COX-2 selectivity and potency of a new class of COX-2 inhibitors". European Journal of Pharmacology. 588 (1 ... instrumental in the elaboration of the COX-2 inflammatory pathway and in the discovery of inhibitors of COX-2, such as ... Mechanism of inhibition of novel COX-2 inhibitors. Gierse J, Kurumbail R, Walker M, Hood B, Monahan J, Pawlitz J, Stegeman R, ... 2002;507:365-9. The novel benzopyran class of selective cyclooxygenase-2 inhibitors-part I: the first clinical candidate. Wang ...
Matveyenko AV, Dry S, Cox HI, et al. (July 2009). "Beneficial endocrine but adverse exocrine effects of sitagliptin in the ... There have been case reports of pancreatitis associated with DPP-4 inhibitors. A group at UCLA reported increased pre-cancerous ... inhibitor class of drugs. Vildagliptin inhibits the inactivation of GLP-1 and GIP by DPP-4, allowing GLP-1 and GIP to ... Dipeptidyl peptidase-4 inhibitors, Pyrrolidines, Nitriles, Novartis brands, Carboxamides, Adamantanes, Tertiary alcohols). ...
Cox, Caroline. "DCPA (Dachtal)". Journal of Pesticide Reform. Archived from the original on 12 July 2010. Retrieved 29 March ... The key difference between DCPA and other mitotic inhibitors is that it often produces multinucleate cells. It essentially ... Cox, Caroline. "DCPA (Dacttal)". Archived from the original on 12 July 2010. Retrieved 18 March 2015. "Disruption of Mitosis" ( ... Cox, Caroline. "DCPA (Dacthal)". Archived from the original on 2010-07-12. Retrieved 2015-03-18. "Dimethyl ...
Nelson DL, Cox M (2021). Lehninger Principles of Biochemistry (8 ed.). Austin. ISBN 978-1-319-22800-2. OCLC 1243000176. The ... though is a more potent inhibitor of growth hormone, glucagon, and insulin than the natural hormone, and has a much longer half ...
Other sites of inhibitor binding have been identified in the human Kinesin-5 motor domain. For inhibitors that bind to the L5 ... PMID 20031160.{{cite journal}}: CS1 maint: uses authors parameter (link) Cox CD, Breslin MJ, Mariano BJ, Coleman PJ, Buser CA, ... The L5 loop in human Kinesin-5 closes around the inhibitor and is open in the absence of inhibitor. These structural changes ... inhibitors. Part 1: The discovery of 3,5-diaryl-4,5-dihydropyrazoles as potent and selective inhibitors of the mitotic kinesin ...
Twells RC, Metzker ML, Brown SD, Cox R, Garey C, Hammond H, Hey PJ, Levy E, Nakagawa Y, Philips MS, Todd JA, Hess JF (Mar 2001 ... Another study found that a different Tph1-inhibitor decreased serotonin levels in the blood and intestine, but did not affect ... Hey PJ, Twells RC, Phillips MS, Brown SD, Kawaguchi Y, Cox R, Dugan V, Hammond H, Metzker ML, Todd JA, Hess JF (Aug 1998). " ...
Aspirin has been found to reduce the risk of death from cancer by about 7%. COX-2 inhibitors may decrease the rate of polyp ... "Nonsteroidal anti-inflammatory drugs and cyclooxygenase-2 inhibitors for primary prevention of colorectal cancer: a systematic ... Angiogenesis inhibitors were once incorrectly thought to have potential as a "silver bullet" treatment applicable to many types ... Angiogenesis inhibitors and other cancer therapeutics are used in combination to reduce cancer morbidity and mortality. ...
Lee, D; Cuendet, M; Vigo, JS; Graham, JG; Cabieses, F; Fong, HH; Pezzuto, JM; Kinghorn, AD (2001). "A novel cyclooxygenase- ... is a naturally occurring protein-tyrosine kinase inhibitor". Biochem. Biophys. Res. Commun. 165 (1): 241-5. doi:10.1016/0006- ...
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 ...
1991). "Use of d-erythro-sphingosine as a pharmacologic inhibitor of protein kinase C in human platelets". Biochem. J. 278 (2 ... 2003). "The sphingosine kinase 1/sphingosine-1-phosphate pathway mediates COX-2 induction and PGE2 production in response to ... Prostaglandins are formed through oxidation of arachidonic acid by cyclooxygenases and other prostaglandin synthases. There are ... histone deacetylase inhibitors and paclitaxel. In some studies, SMase activation results to its transport to the plasma ...
Oncolytics is conducting its first study of REOLYSIN in combination with a checkpoint inhibitors in an open-label phase 1b ... Duncan, MR; Stanish, SM; Cox, DC (1978). "Differential sensitivity of normal and transformed human cells to reovirus infection ...
Involved in the mechanism of action is inhibition of cyclooxygenase (COX-1 and COX-2) which leads to the potential adverse ... anti-platelet agents and selective serotonin reuptake inhibitors (SSRIs), tacrolimus, zidovudine, and gold/penicillamine. Like ...
Those that are specific to the COX-2 isozyme are called COX-2 inhibitors. The active metabolite (AM404) of paracetamol is a COX ... in human hepatocellular carcinoma Cyclooxygenase 1 Cyclooxygenase 2 Discovery and development of COX-2 selective inhibitors COX ... The main COX inhibitors are the non-steroidal anti-inflammatory drugs. The classical COX inhibitors are not selective and ... Because COX-2 is usually specific to inflamed tissue, there is much less gastric irritation associated with COX-2 inhibitors, ...
Dan Kusnetzky, cloud computing analyst at research firm the 451 group cites resistance to change as an inhibitor to cloud ... "HP takes the wraps off cloud-focused channel program," CRN, March 29, 2011 [12] Cox, Mark. "HP announces new program for ...
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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-2 (COX-2) inhibitors. Class Summary. Although increased cost can be a negative factor, COX-2 inhibitors may be ... COX-2 inhibitors and many traditional NSAIDs may increase the risk of atherosclerotic cardiovascular endpoints. ... Inhibition of COX-1 may contribute to NSAID GI toxicity. At therapeutic concentrations, COX-1 isoenzyme is not inhibited; thus ... Phosphodiesterase (type 5) enzyme inhibitor. Class Summary. Phosphodiesterase inhibitors can ameliorate symptoms of pulmonary ...
Cyclo-oxygenase 2 Inhibitors. Class Summary. COX-2 inhibitors are used to control pain and inflammation, especially in cases of ... Ongoing analysis of cost avoidance of GI bleeds will further define the populations that will find COX-2 inhibitors the most ... Inhibition of COX-1 may contribute to NSAID GI toxicity, but at therapeutic concentrations, COX-1 isoenzyme is not inhibited ... Fenoprofen decreases the formation of prostaglandin precursors by inhibiting cyclooxygenase (COX)-1 and 2 enzymes. It may also ...
... J Nat ... COX-1, and COX-2. It was found that 3-O-acetyl-β-boswellic acid potently inhibited human 15-LOX-2 (IC50 = 12.2 ± 0.47 μM). ... Notably, the introduction of a carboxylic acid group at position 30 was important for dual 5-LOX/COX inhibitory activity; ... relationships revealed that the presence of a hydroxy group at position 24 was beneficial in terms of both 5-LOX and COX-1 ...
Avoid COX-2 inhibitors in patients with active gastroduodenal disease. COX-2 inhibitors should not be prescribed to patients ... Gastrointestinal toxicity reduced by COX-2 inhibitors but not abolished. The COX-2 inhibitors exert their therapeutic effect by ... Adverse reaction reports and epidemiological studies suggest that cyclo-oxygenase-2 (COX-2) inhibitors cause gastroduodenal ... Where strongly indicated, COX-2 inhibitors may be prescribed to patients with a past history of gastroduodenal disease, and ...
COX-2 inhibitors are also prime candidates for preventing cancer or its recurrence. Gary J. Kelloff, chief of the ... chemoprevention branch at the National Cancer Institute (NCI), lists the requirements for a molecular target such as the COX-2 ... "COX-2 is an ideal target," he says. The COX-2 inhibitors shot to pharmaceutical fame in December 1998, when the Food and Drug ... COX-2 Inhibitors Tackle Cancer. Image: Courtesy of Hibiki Kawamata, Smith College A drug developers dream, rationally designed ...
COX-2 selektivni inhibitor je forma steroidnog antiinflamatornog leka (NSAID) koji direktno deluju na COX-2, enzim koji je ... Malhotra S, Shafiq N, Pandhi P (2004). „COX-2 Inhibitors: A CLASS Act or Just VIGORously Promoted". MedGenMed 6 (1): 6. PMC ... National Trends in Cox-2 inhibitor use since market release: non-selective diffusion of a selectively cost-effective innovation ... and selective COX-2 inhibitors in the treatment of symptomatic knee osteoarthritis". Value Health 6 (2): 144-57. DOI:10.1046/j. ...
... selective COX-3 inhibitor. Quality confirmed by NMR & HPLC. See customer reviews, validations & product citations. ... Ketorolac is a non-selective COX inhibitor of COX-1 and COX-2 with IC50 of 1.23 μM and 3.50 μM, respectively. ... Other COX Products. * XanthohumolNew. Xanthohumol, a prenylated chalcone from hop, inhibits COX-1 and COX-2 activity and shows ... Lornoxicam (Chlortenoxicam) is a non-steroidal COX-1/COX-2 inhibitor, used as an anti-inflammatory drug to treat pain, ...
... about Cox-2 Inhibitors and the controversy surrounding these popular drugs which are often prescribed to pain patients. ... COX-2 inhibitors vs traditional NSAIDs.. While the therapeutic strength of COX-2 inhibitors lies in their ability to reduce ... Two COX forms, COX-1 and COX-2, were uncovered. COX-1 enzymes are normally found in most tissues and protect the stomach lining ... In 1971, pharmacologist John Vane showed that aspirin stops the action of an enzyme called cyclooxygenase, or COX. COX plays a ...
Cyclooxygenase inhibitors - Reference pathway ...
Cyclooxygenase-2: potential role in regulation of drug efflux and multidrug resistance phenotype. Sorokin A... ... existence of causal link between Cox-2 activity and MDR1 expression. The use of Cox-2 inhibitors to. decrease function of MDR1 ... Anti-cancer potency of cyclooxygenase. inhibitors is established, but the mechanism of Cox-2-dependent potentiation of tumor ... Cyclooxygenase-2: potential role in regulation of drug efflux and multidrug resistance phenotype.. Sorokin A.. Department of ...
Cox-2 Inhibitors and Cancer. As a person who has an arthritic condition I can tell you that when the cox-2 inhibitors first ... When coupled with cox-2 inhibitors the morphine not only provided better analgesic effects (better pain control), but also ... Personally, I will ask my doctor to add cox-2 inhibitors to my drug regime to control pain and hopefully decrease tumor load. ... At my last visit with my rheumatologist directed me to cut back by half my consumption of cox-2 inhibitors. With great ...
Check COX pathway , inhibitors reviews and assay information. ... COX Inhibitors on signaling pathway are available at Adooq ... COX-1/COX-2 inhibitor Aspirin is a non-selective and irreversible inhibitor of COX-1 and COX-2 with IC50s of 5 and 210 μg/mL. ... COX inhibitor Piroxicam is an effective and potent inhibitor of prostaglandin synthesis and a Cox-1 and Cox-2 inhibitor. Learn ... COX inhibitor Diclofenac Sodium is a non-selective COX inhibitor with IC50 of 0.5 μg/ml and 0.5 μg/ml for COX-1 and -2 in ...
The Case of Cox-2 Inhibitors by Craig L. Garthwaite. Published in volume 4, issue 3, pages 116-37 of American Economic Journal ... This study estimates the labor supply effects of Cox-2 inhibitors, a widely prescribed class of pharmaceuticals used for the ... The Economic Benefits of Pharmaceutical Innovations: The Case of Cox-2 Inhibitors. * Craig L. Garthwaite ... The Economic Benefits of Pharmaceutical Innovations: The Case of Cox-2 Inhibitors ...
Luderer, J. R. ; Demers, L. ; Nomides, C. / Levamisole is a reversible cyclooxygenase inhibitor in vitro. In: Clinical ... Luderer, J. R., Demers, L., & Nomides, C. (1981). Levamisole is a reversible cyclooxygenase inhibitor in vitro. Clinical ... Luderer JR, Demers L, Nomides C. Levamisole is a reversible cyclooxygenase inhibitor in vitro. Clinical pharmacology and ... Luderer, JR, Demers, L & Nomides, C 1981, Levamisole is a reversible cyclooxygenase inhibitor in vitro, Clinical pharmacology ...
Cyclooxygenase inhibitors represented extremely promising novel anti-inflammatory drugs until one of them, rofecoxib (Vioxx), ... An Ion Channel Hypothesis to Explain Divergent Cardiovascular Safety of Cyclooxygenase-2 Inhibitors: The Answer to a Hotly ... An Ion Channel Hypothesis to Explain Divergent Cardiovascular Safety of Cyclooxygenase-2 Inhibitors: The Answer to a Hotly ... An Ion Channel Hypothesis to Explain Divergent Cardiovascular Safety of Cyclooxygenase-2 Inhibitors: The Answer to a Hotly ...
Treating Discogenic Pain by Reducing Dorsal Root Ganglion Cell Sensitization using the COX-2 Inhibitor Celecoxib - An in vitro ... Treating discogenic pain by reducing nerve sensitization and ingrowth using the COX-2 inhibitor celecoxib - an in vitro study ... Can the COX-2 inhibitor Celecoxib influence discogenic pain signals? An in vitro study with inflamed annulus fibrosus cells. ... Can the COX-2 inhibitor Celecoxib influence discogenic pain signals? An in vitro study with inflamed annulus fibrosus cells. ...
Intrathecal Cyclooxygenase Inhibitors in Humans: Dont Throw in the Towel! Martin S. Angst, M.D. Martin S. Angst, M.D. ... It is too early to throw in the towel on the potential utility of intrathecal cyclooxygenase inhibitors in the management of ... Martin S. Angst; Intrathecal Cyclooxygenase Inhibitors in Humans: Dont Throw in the Towel!. Anesthesiology 2010; 112:1082-1083 ... We have learned from these seminal studies that intrathecal cyclooxygenase inhibitors are not a panacea for all types of pain. ...
COX-2 inhibitors are non-steroidal anti-inflammatory drugs (NSAIDs) commonly used for osteoarthritis and rheumatoid arthritis ... COX-2 inhibitors work by blocking the action of an enzyme called cyclooxygenase-2, which produced prostaglandins. ... COX-2 inhibitors are a type of non-steroidal anti-inflammatory drug commonly used in the treatment of osteoarthritis and ... Currently, the only COX-2 inhibitor available in the United States is celecoxib (Celebrex). ...
COX inhibitor , CAS [53-86-1] , Axon 3318 , Axon Ligand™ with >99% purity available from supplier Axon Medchem, prime source of ... KEYWORDS: Indomethacin , COX inhibitor , CAS [53-86-1] , Fatty acid (Arachidonic acid) , COX , Inhibitor , Enzymes ... Indomethacin is a potent, time-dependent, nonselective inhibitor of the cyclooxygenase enzymes (COX-1 and COX-2). Indomethacin ... COX-inhibitor; NSAID Chemical name. 2-(1-(4-Chlorobenzoyl)-5-methoxy-2-methyl-1H-indol-3-yl)acetic acid ...
Only a few COX-1-selective inhibitors are currently available, and the research on COX-1 selective inhibitors is not fully ... N2 - Only a few COX-1-selective inhibitors are currently available, and the research on COX-1 selective inhibitors is not fully ... AB - Only a few COX-1-selective inhibitors are currently available, and the research on COX-1 selective inhibitors is not fully ... abstract = "Only a few COX-1-selective inhibitors are currently available, and the research on COX-1 selective inhibitors is ...
Cyclooxygenase (COX-2) inhibitors were developed with the hope that they will cause fewer gastrointestinal adverse effects. ... Comparative gastrointestinal toxicity of selective cyclooxygenase (COX-2) inhibitors.. Authors: Shafiq, N. Malhotra, S. Pandhi ... Shafiq N, Malhotra S, Pandhi P, Nada R. Comparative gastrointestinal toxicity of selective cyclooxygenase (COX-2) inhibitors. ... Ability of selective as well as nonselective COX inhibitors to alter ischemia-reperfusion induced damage of gastric mucosa and ...
74 Cyclooxygenase Inhibitors: Nonsteroidal Antiinflammatory Drugs and Acetaminophen for Nursing RN faster and easier with ... COX Inhibitor. Indications. General Pain. Fever. Inflammatory Conditions. Side Effects. GI Ulcers. Nephrotoxicity. Rash. ... 74 - Cyclooxygenase Inhibitors: Nonsteroidal Antiinflammatory Drugs and Acetaminophen. 9. Picmonics to Learn , 13 mins ... Reversible Inhibition of COX-1 and COX-2. Block Prostaglandin Synthesis. Side Effects. Interstitial Nephritis. Gastric Ulcer. ...
Cyclo-oxygenase-2 Inhibitors. Class Summary. Although increased cost can be a negative factor, the incidence of costly and ... Primarily inhibits COX-2. COX-2 is considered an inducible isoenzyme; it is induced by pain and inflammatory stimuli. The ... Their mechanism of action is not known, but they may inhibit cyclo-oxygenase (COX) activity and prostaglandin synthesis. Other ... At therapeutic concentrations, COX-1 isoenzyme is not inhibited; thus, the incidence of GI toxicity, such as endoscopic peptic ...
Cyclo-oxygenase-2 Inhibitors. Class Summary. Although increased cost can be a negative factor, the incidence of costly and ... Primarily inhibits COX-2. COX-2 is considered an inducible isoenzyme; it is induced by pain and inflammatory stimuli. The ... Their mechanism of action is not known, but they may inhibit cyclo-oxygenase (COX) activity and prostaglandin synthesis. Other ... At therapeutic concentrations, COX-1 isoenzyme is not inhibited; thus, the incidence of GI toxicity, such as endoscopic peptic ...
Tag: cox 2 inhibitors. Easing the pain of migraine attacks. May 14, 2012. May 14, 2012. ... probably aware of the gastrointestinal and cardiovascular side-effects associated with NSAIDs and selective COX-2 inhibitors - ... Posts about cox 2 inhibitors written by Editor ...
Role of COX-2 inhibitors in cancer therapy. / Blanke, Charles.. In: Cancer Investigation, Vol. 22, No. 2, 2004, p. 271-282.. ... Role of COX-2 inhibitors in cancer therapy. In: Cancer Investigation. 2004 ; Vol. 22, No. 2. pp. 271-282. ... Role of COX-2 inhibitors in cancer therapy. Cancer Investigation. 2004;22(2):271-282. doi: 10.1081/CNV-120030216 ... Blanke, C. (2004). Role of COX-2 inhibitors in cancer therapy. Cancer Investigation, 22(2), 271-282. ...
  • Although increased cost can be a negative factor, COX-2 inhibitors may be more effective in reducing the incidence of costly and potentially fatal GI bleeding than traditional NSAIDs. (
  • COX-2 inhibitors and many traditional NSAIDs may increase the risk of atherosclerotic cardiovascular endpoints. (
  • Will the promise of the COX-II selective NSAIDs come to fruition? (
  • Traditional NSAIDs, like aspirin, block both COX forms. (
  • It is easy to forget two important points about COX-2 inhibitors vs. traditional NSAIDs: they both have the same effectiveness, and they both can cause side effects related to blood pressure, liver, and kidney problems. (
  • Most people are probably aware of the gastrointestinal and cardiovascular side-effects associated with NSAIDs and selective COX-2 inhibitors - if you are not, just Google Vioxx or Celebrex! (
  • The major effect of all NSAIDs is to decrease the synthesis of prostaglandins by reversibly inhibiting cyclooxygenase (COX), an enzyme that catalyzes the formation of prostaglandins and thromboxanes from the precursor, arachidonic acid. (
  • Classic, older NSAIDs (eg, ibuprofen) inhibit COX-1 more than COX-2, whereas the newer class of NSAIDs (eg, celecoxib) inhibit COX-2 predominantly, decreasing gastrointestinal adverse effects. (
  • The cyclo-oxygenase 2 (COX-2) inhibitors are a new form of non-steroidal anti-inflammatory drugs (NSAIDs) that are considered to produce fewer gastro-intestinal side effects than the older non-selective drugs. (
  • A new class of NSAIDs, COX2 selective inhibitors (Coxibs), have been developed with the aim of reducing the GI adverse events of traditional NSAIDs while maintaining their effective anti-inflammatory and analgesic properties. (
  • OBJECTIVE: We conducted a case/noncase analysis of spontaneous reports to compare the hepatic safety profile of cyclooxygenase (COX)-2 selective inhibitors with that of nonselective NSAIDs. (
  • The PRs of hepatic disorders for all COX-2 selective inhibitors and non-selective NSAIDs were 3.0% in the FDA/FOI database and 2.7% in the WHO/UMC database. (
  • Two review studies evaluating the safety of the selective cyclooxygenase 2 ( COX-2 ) inhibitors and non-steroidal anti-inflammatory drugs ( NSAIDs ) have found increased cardiovascular and kidney risks. (
  • The authors based their analysis on 17 case-control analyses that included 86,193 cases with cardiovascular events and over 500,000 controls, and six cohort analyses that included 75,520 users of selective COX-2 inhibitors, 375,619 users of non-selective NSAIDs, and nearly 600,000 unexposed participants. (
  • Inhibitors selective for prostaglandin G/H synthase-2 (PGHS-2) (known colloquially as COX-2) were designed to minimize gastrointestinal complications of traditional NSAIDs - adverse effects attributed to suppression of COX-1-derived PGE 2 and prostacyclin (PGI 2 ). (
  • NSAIDs, which include both traditional NSAIDs (tNSAIDs) and selective inhibitors of COX-2 and which are among the most commonly used drugs ( 5 ), relieve pain and inflammation by suppressing the COX function of PGHS and the consequent formation of PGE 2 ( 6 ) and prostacyclin (PGI 2 ) ( 7 ), but perhaps also of other prostanoids. (
  • Non-selective NSAIDS and selective COX-2 inhibitors appear to carry similar risks [ 5 ]. (
  • Since prostaglandins are synthesized by the COX enzymes, COX inhibitors like the NSAIDs should have the potential to impair this process. (
  • On the other hand, inhibition from the COX pathway by NSAIDs may shunt the rate of metabolism of arachidonic acidity into the additional path, i.e., activating the lipoxygenase (5-LOX) pathway. (
  • This system continues to be disputed because particular NSAIDs that trigger enteropathy usually do not just inhibit COX but also regulate 5-LOX. (
  • Meloxicam: The mechanism of action of meloxicam, like that of other NSAIDs, is not completely understood but involves inhibition of cyclooxygenase (COX-1 and COX-2). (
  • The COX-2 inhibitors shot to pharmaceutical fame in December 1998, when the Food and Drug Administration approved Celebrex (celecoxib) to treat osteoarthritis and rheumatoid arthritis. (
  • Celecoxib (Celebrex, Celebra,SC 58635) is a selective COX-2 inhibitor with IC50 of 40 nM in Sf9 cells. (
  • In pain-management of LBP, nonsteroidal anti-inflammatory drugs (NSAID) and specific cyclooxygenase-2 blocker, like celecoxib, are often prescribed for an oral use and have many side effects. (
  • Treating Discogenic Pain by Reducing Dorsal Root Ganglion Cell Sensitization using the COX-2 Inhibitor Celecoxib - An in vitro Study with Inflammatory Cytokine Treated Annulus Fibrosus Cells. (
  • Häckel S, Häne S, Eglauf J, Ma J, Pfannkuche J, Hoppe S, Albers C, Grad S. Die modulierende Wirkung des Cyclooxygenase-2 Inhibitors Celecoxib auf diskogenen Schmerz - eine in vitro Studie mit humanen Annulus fibrosus Zellen. (
  • Currently, the only COX-2 inhibitor available in the United States is celecoxib (Celebrex). (
  • The model compound for the study is the nonsteroidal anti-inflammatory drug celecoxib, a COX-2 selective inhibitor and known CYP2C9 substrate. (
  • Nevertheless, the selective COX-2 inhibitor, celecoxib (which didn't trigger enteropathy in wild-type pets), triggered ulceration in the tiny intestine of mice (Sigthorsson knockout mice exhibited little intestinal ulcers although these were not really serious (Sapirstein and Bonventre, 2000). (
  • Inhibits inflammatory reactions and pain by decreasing enzyme COX activity, which results in prostaglandin synthesis. (
  • Diclofenac inhibits prostaglandin synthesis by decreasing the activity of the enzyme cyclooxygenase, which in turn decreases the formation of prostaglandin precursors. (
  • Bacopa reduces inflammation by positively modulating COX and LOX enzyme pathways and Tumor Necrosis Factor. (
  • In 1971, pharmacologist John Vane showed that aspirin stops the action of an enzyme called cyclooxygenase, or COX. (
  • Etoricoxib specifically binds to and inhibits the enzyme cyclooxygenase-2 (COX-2), resulting in inhibition of the conversion of arachidonic acid into prostaglandins. (
  • COX-2 inhibitors work by blocking the action of an enzyme called cyclooxygenase-2, which produced prostaglandins. (
  • Nonacidic NSAID that is rapidly metabolized after absorption, becoming a major active metabolite that inhibits the COX enzyme (thereby inhibiting pain and inflammation). (
  • With decreased risk of adverse gastrointestinal effects, a class of drugs that selectively inhibits COX-2 enzyme was introduced for analgesia and the treatment of arthritis. (
  • They block a specific enzyme , COX-2, that's responsible for making prostaglandins, chemicals that trigger inflammation or pain. (
  • It acts as an inhibitor of the COX-2 enzyme which is responsible for pain and inflammation. (
  • 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. (
  • Fortunately, frankincense extract has proved an effective inhibitor against this enzyme. (
  • It has been suggested that angiotensin converting enzyme inhibitors (ACE-1 inhibitors), such as enalapril and ramipril, and angiotensin receptor antagonists (colloquially called angiotensin receptor blockers or ARBs), such as candesartan and valsartan, may be of value in preventing and treating the effects of the coronavirus SARS-CoV-2 (also known as 2019-nCoV), the cause of the infection called COVID-19. (
  • 11] Cox is an enzyme that the body produces during an inflammatory response. (
  • Inhibition of COX-1 may contribute to NSAID GI toxicity. (
  • Inhibition of COX-1 may contribute to NSAID GI toxicity, but at therapeutic concentrations, COX-1 isoenzyme is not inhibited and thus, GI toxicity may be decreased. (
  • COX-2 selektivni inhibitor je forma steroidnog antiinflamatornog leka (NSAID) koji direktno deluju na COX-2 , enzim koji je odgovoran za inflamaciju i bol . (
  • COX-2 selektivnost ne umanjuje druge nepoželjne efekte NSAID lekova (pogotovu povišeni rizik od bubrežne insuficijencije ), a rezultati nekih istraživanja ukazuju i na povišeni rizik od srčanog udara , tromboze i moždanog udara kao posledica relativnog povišenja nivoa tromboksana . (
  • FK3311 is a cell-permeable and orally available sulfonanilide that acts as a selective COX-2 inhibitor and NSAID. (
  • Ibuprofen is a nonsteroidal anti-inflammatory drug (NSAID) targeting COX-1 with an IC50 of 13 μM. (
  • The result of NSAID-induced COX inhibition is decreased production of prostaglandins, which leads to decreased pain and inflammation. (
  • Piroxicam is an NSAID and, as such, is a non-selective COX inhibitor possessing both analgesic and antipyretic properties. (
  • Among these, a book strategy already shown inside a murine model may be the selective disruption of bacteria-specific -glucuronidases having a book little molecule inhibitor that will not harm the bacterias which alleviates NSAID-induced enteropathy. (
  • Analysis of the structure-activity relationships revealed that the presence of a hydroxy group at position 24 was beneficial in terms of both 5-LOX and COX-1 inhibition. (
  • Inhibition of COX-2 may induce apoptosis and inhibit tumor cell proliferation and angiogenesis. (
  • 1 Studies in animals further suggest that intrathecal injections of cyclooxygenase inhibitors attenuate both the concentration of spinal prostaglandins and nociceptive behavior, implying that targeted inhibition of spinal cyclooxygenase may be a viable strategy for treating pain in humans. (
  • According to the authors, the adverse renal effects of selective COX-2 inhibition are unclear. (
  • IL-1 release however is not effectively neutralized by cyclooxygenase inhibition. (
  • The clinical information is biologically plausible, as it is compatible with evidence that inhibition of COX-2-derived PGI 2 removes a protective constraint on thrombogenesis, hypertension, and atherogenesis in vivo. (
  • COX inhibition can lead to decreased sodium excretion and increased sodium retention. (
  • Fenoprofen decreases the formation of prostaglandin precursors by inhibiting cyclooxygenase (COX)-1 and 2 enzymes. (
  • The inhibitory activities of 29 natural oleanane and ursane pentacyclic triterpenes were evaluated against four major enzymes involved in the inflammatory process: 5-LOX, 15-LOX-2, COX-1, and COX-2. (
  • COX-1 enzymes are normally found in most tissues and protect the stomach lining. (
  • In contrast, COX-2 enzymes become active when the body senses pain and responds by promoting inflammation. (
  • Indomethacin is a potent, time-dependent, nonselective inhibitor of the cyclooxygenase enzymes (COX-1 and COX-2). (
  • COX-2 has a sulfonamide chain and is primarily dependent on cytochrome P450 enzymes (hepatic enzymes) for metabolism. (
  • This means that its purpose is to block both of the enzymes (COX 1 and COX 2) that are responsible for the production of prostaglandins, a chemical that causes the pain and swelling as an immune response to injury. (
  • commonly known as COX) enzymes, lipoxygenases, and epoxygenases to form a mesmerizing array of biologically active products. (
  • The COX enzymes are bisfunctional proteins, possessing both COX and hydroperoxidase (HOX) activities, catalyzing the biotransformation of AA into the PG endoperoxide intermediates PGG 2 and PGH 2 . (
  • Cyclooxygenase enzymes, which regulate the conversion of arachidonic acid to prostaglandins, are abundantly present in the kidneys and play an important role in renal hemostasis, renin release, renal tubular salt and water reabsorption. (
  • Nuclear-Factor-Kappa Beta, Cox enzymes, Interleukin-1β, MMP-13, and MMP-2, are all biological agents involved in the inflammatory process that can lead to arthritis, cancer, and Alzheimer's disease. (
  • Inhibits primarily COX-2, which is considered an inducible isoenzyme (ie, induced during pain and inflammatory stimuli). (
  • This agent inhibits inflammatory reactions and pain by decreasing the activity of cyclooxygenase, which results in a decrease of prostaglandin synthesis. (
  • Sulindac decreases the activity of cyclooxygenase and in turn inhibits prostaglandin synthesis. (
  • Xanthohumol, a prenylated chalcone from hop, inhibits COX-1 and COX-2 activity and shows chemopreventive effects. (
  • Primarily inhibits COX-2. (
  • This is in contrast to salicylates (eg, aspirin), which irreversibly bind to COX and inhibit production for the entire life of the cell, or acetaminophen, which inhibits COX centrally. (
  • inhibits cyclooxygenase (COX), an early component of the arachidonic acid cascade, resulting in reduced synthesis of prostaglandins, thromboxanes, and prostacyclin. (
  • Within an exercise context, banana metabolites that increase in the blood following ingestion have a similar effect to aspirin or ibuprofen that inhibits COX-2 activity. (
  • At what care level are cyclo-oxygenase-2 inhibitors prescribed? (
  • Phosphodiesterase inhibitors, endothelin receptor antagonists, or prostaglandins can be used for pulmonary hypertension. (
  • The COX-2 inhibitors exert their therapeutic effect by inhibiting the production of prostaglandins involved in inflammation. (
  • THE role of spinal cyclooxygenase and prostaglandins in nociceptive processing has been examined, corroborated, and reported in more than 100 publications describing animal and bench studies during the past 3 decades. (
  • Relevant observations include the constitutive expression of cyclooxygenase 1 and 2 in the spinal cord, up-regulation of cyclooxygenase 2 (primarily) and cyclooxygenase 1 after peripheral injury, release and production of spinal prostaglandins in response to tonic and often inflammatory nociceptive input, and an association between an increase in spinal prostaglandins and nociceptive behavior. (
  • This paradoxic ulcer and colitis aggravating effect of selective COX-2 inhibitors may be explained by suppression of protective prostaglandins generated as a consequence of COX-2 induction in inflammatory states. (
  • Cyclooxygenase-1 (COX-1) has been proposed to generate prostaglandins that maintain organ function, protect the integrity of the gastric mucosa, and generate platelet-derived thromboxane responsible for platelet aggregation and vasoconstriction. (
  • Cyclooxygenase-2 (COX-2) is induced during the inflammatory response and produces prostaglandins that mediate pain and inflammation. (
  • It contains etoricoxib, a selective inhibitor of cyclooxygenase-2 (COX-2), which blocks the formation of prostaglandins, substances responsible for inflammation, pain and fever symptoms. (
  • Because meloxicam is an inhibitor of prostaglandin synthesis, its mode of action may be due to a decrease of prostaglandins in peripheral tissues. (
  • Indomethacin (NSC-77541, Indometacin) 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. (
  • Ability of selective as well as nonselective COX inhibitors to alter ischemia-reperfusion induced damage of gastric mucosa and hapten-induced colitis in rats has been compared. (
  • COX-2 inhibitors are used to control pain and inflammation, especially in cases of contraindication to conventional anti-inflammatories. (
  • Image: Courtesy of Hibiki Kawamata, Smith College A drug developer's dream, rationally designed to quell inflammation, COX-2 inhibitors are also prime candidates for preventing cancer or its recurrence. (
  • This study estimates the labor supply effects of Cox-2 inhibitors, a widely prescribed class of pharmaceuticals used for the treatment of chronic pain and inflammation and primarily marketed under the brand names Vioxx, Celebrex, and Bextra. (
  • A reduction in COX-2 mRNA expression usually results in less inflammation and reduced swelling and the perception of pain. (
  • Unlike COX-1, which appeared to be expressed constitutively in most tissues, COX-2 was subject to rapid induction by inflammatory cytokines and mitogens and was speculated to account largely if not exclusively for PG formation in inflammation and cancer. (
  • The cyclooxygenase inhibitor, ibuprofen, significantly inhibited the LPS-induced rise in PGE2, TXB2 and TNF but had only a modest suppressive effect on IL-1 release. (
  • Lornoxicam (Chlortenoxicam) is a non-steroidal COX-1/COX-2 inhibitor, used as an anti-inflammatory drug to treat pain, osteoarthritis, and rheumatoid arthritis. (
  • Aspirin (NSC 27223, Acetylsalicylic acid, ASA) is a salicylate, and irreversible COX1 and COX2 inhibitor, used as an analgesic to relieve minor aches and pains, as an antipyretic to reduce fever, and as an anti-inflammatory medication. (
  • Naproxen sodium is a non-selective cyclooxygenase (COX) inhibitor that displays anti-inflammatory, antipyretic and analgesic effects. (
  • COX-2 inhibitors are a type of non-steroidal anti-inflammatory drug commonly used in the treatment of osteoarthritis and rheumatoid arthritis . (
  • The mechanism of action of these agents is not known, but they may inhibit cyclooxygenase activity and prostaglandin synthesis. (
  • Their mechanism of action is not known, but they may inhibit cyclo-oxygenase (COX) activity and prostaglandin synthesis. (
  • Their mechanism of action is not known, but may inhibit cyclooxygenase activity and prostaglandin synthesis. (
  • Meloxicam is a potent inhibitor of prostaglandin synthesis in vitro. (
  • Evidence is accumulating on the potential class effect of COX-2 inhibitors on cardiovascular risk. (
  • Stroke and Heart Attack: A Class Effect of COX 2 Inhibitors? (
  • Many of the synthesized agents show enhanced COX-1/2 properties than aspirin with better selectivity index towards COX-2 relative to COX-1. (
  • Protective effects of etoricoxib, a selective inhibitor of cyclooxygenase-2, in experimental periodontitis in rats. (
  • As with NSAIAs, COX-2 inhibitors should be withdrawn in patients with significant gastrointestinal symptoms, pending investigation. (
  • Gastrointestinal adverse effects account for about 30% of the COX-2 inhibitor reactions reported to the Centre for Adverse Reactions Monitoring (CARM). (
  • IMSEAR at SEARO: Comparative gastrointestinal toxicity of selective cyclooxygenase (COX-2) inhibitors. (
  • Shafiq N, Malhotra S, Pandhi P, Nada R. Comparative gastrointestinal toxicity of selective cyclooxygenase (COX-2) inhibitors. (
  • Cyclooxygenase (COX-2) inhibitors were developed with the hope that they will cause fewer gastrointestinal adverse effects. (
  • The synthesized conjugates can be considered as multi-targeted tyrosine kinase inhibitors due to the promising properties against VEGFR-2 and EGFR in MCF7 and HCT116. (
  • During tumor-associated angiogenesis, the balance of angiogenesis stimulators and inhibitors is tipped in favor of angiogenesis by hypoxia-inducible factor-1 gene expression [ 2 ]. (
  • In the 1990s, we cloned the inducible cyclooxygenase (COX-2) and the first S1P receptor. (
  • Our observation that cyclopamine acts independently of Smo to disrupt zebrafish PGC migration is also surprising, as this small molecule has been used AZD1480 JAK inhibitor extensively to study Hh pathway dependent patterning in this model organism. (
  • Our work defined how the COX-2 pathway regulated angiogenesis, cancer and inflammatory disease. (
  • Flurbiprofen may inhibit COX, thereby inhibiting prostaglandin biosynthesis. (
  • In a new study completed by Appalachian State University's Human Performance Laboratory and published March 22 in the scientific journal PLOS ONE , both were found to inhibit COX-2 mRNA expression. (
  • ACE-1 inhibitors inhibit the conversion of angiotensin I to angiotensin II and of angiotensin(1-9) to angiotensin(1-7). (
  • Treatment for necrotizing scleritis was started with 0.5% cyclosporine eyedrops, corticosteroids, and systemic cyclooxygenase 2 inhibitor. (
  • Surgical versus medical treatment with cyclooxygenase inhibitors for symptomatic patent ductus arteriosus in preterm infants. (
  • Rofecoxib (MK-0966) is a COX-2 inhibitor with IC50 of 18 nM. (
  • In this comprehensive meta-analysis of 114 randomized trials of COX-2 inhibitors comprised of 116,094 participants, Rofecoxib uniquely increased risks of renal events ( peripheral edema, renal dysfunction, hypertension ) and arrhythmia events, with apparent adverse effects by the end of year 2000 and 2004, respectively," the researchers write. (
  • AZD3839 is a potent and selective BACE1 inhibitor with K i of 26.1 nM, about 14-fold selectivity over BACE2. (
  • Thus was born a new line of pain management drugs called selective COX-2 inhibitors. (
  • The use of Cox-2 inhibitors to decrease function of MDR1 may enhance accumulation of chemotherapy agents and decrease resistance of tumors to chemotherapeutic drugs. (
  • Then came the news that the cox-2 drugs caused coronary issues and doctors were warned to use them with great caution. (
  • Preoperative drugs may include cyclooxygenase-2 (COX-2) inhibitors and opioid analgesic agents. (
  • Study author Dr. Morten Schmidt adds, "While newer versions of these COX-2 inhibitor drugs have been pulled off shelves, older ones are still frequently prescribed. (
  • These drugs are chemically related antiviral medications known as neuraminidase inhibitors that have activity against both influenza A and B viruses. (
  • Only a few COX-1-selective inhibitors are currently available, and the research on COX-1 selective inhibitors is not fully developed. (
  • The authors have produced several COX-1 selective inhibitors including N-(5-amino-2-pyridinyl)-4-trifluoromethylbenzamide: TFAP (3). (
  • This information is useful to design new COX-1 selective inhibitors without colored urine based on the chemical structure of 3. (
  • Evidence from 2 randomized controlled-outcome trials (RCTs) of 2 structurally distinct selective inhibitors of COX-2 supports this hypothesis. (
  • While the therapeutic strength of COX-2 inhibitors lies in their ability to reduce stomach complications, their adverse reactions cannot be overlooked. (
  • Here, these findings are discussed in light of the role of KCNQ K + channels in control of excitability in general, the "lipid imbalance theory" of cyclooxygenase-2 risks, and the potential for novel therapeutic modalities for cardiovascular disease focused on ion channels in vascular smooth muscle. (
  • At therapeutic concentrations, COX-1 isoenzyme is not inhibited thus GI toxicity may be decreased. (
  • ABSTRACT The aim of the study was to assess the accuracy of some specific biochemical indicators in discriminating between Helicobacter pylori-associated gastritis and H. pylori-associated stomach cancer (serum gastrin level, serum soluble E-cadherin and tissue COX-2 activity, as well as serodiagnostic markers for H. pylori infection) in order to find a simple diagnostic test that can reasonably predict the development of gastric cancer. (
  • TCA-9-736-s004.tif (708K) GUID:?80EEED9A-FEAD-48DB-81F3-D2F893D2F19E Abstract Background Strict eligibility criteria for patient enrollment AZD8055 inhibitor database in phase III trials raise questions regarding generalization to AZD8055 inhibitor database ineligible patients. (
  • Case reports suggest that COX-2 inhibitors, like NSAIAs, may exacerbate inflammatory bowel disease and cause intestinal strictures. (
  • Acetaminophen is a potent hepatic N-acetyltransferase 2 (NAT2) inhibitor. (
  • Usually, you alternate a COX-2 inhibitor with acetaminophen, Bolash says. (
  • [ 39 ] The INBUILD trial, which included patients with MCTD, reported that treatment with the antifibrotic tyrosine kinase inhibitor nintedanib can significantly slow the annual rate of decline in forced vital capacity (FVC) in patients with progressive fibrosing interstitial lung diseases. (
  • The most potent inhibitor flavopiridol TEFb P 2 effectively blocked HIV-1 viral replication and Tattransactivation activity t of P TEFb kinase inhibitor in non-cytotoxic concentrations without the cellular Ren transcription. (
  • Their functionally diverse antibodies represent a new class of checkpoint inhibitors that harness both the adaptive and innate immune responses. (
  • It is therefore expected that COX-2 inhibitors will have reduced gastroduodenal toxicity compared with conventional NSAIAs. (
  • Can Patients Stomach COX-2 Inhibitors? (
  • All except two patients had at least one risk factor, other than use of a COX-2 inhibitor, for gastroduodenal ulceration. (
  • It is likely that this observation in part reflects preferential prescribing of COX-2 inhibitors to at-risk patients. (
  • It is not known what degree of risk reduction is achieved when switching high-risk patients from NSAIAs to COX-2 inhibitors. (
  • Patients taking COX-2 inhibitors presently and having a history of a stroke, mini-stroke, coronary heart disease or peripheral arterial disease should review the prescription with their health care provider. (
  • Patients are also advised that though stopping COX-2 inhibitors will not cause any harm, yet they are likely to need alternative treatment to control symptoms. (
  • Jingjing Zhang, from Brigham and Women's Hospital and Harvard Medical School, Boston, and colleagues evaluated the adverse risks of renal events and arrhythmia events in patients prescribed COX-2 inhibitors from a systematic review of the medical literature to determine if these negative side-effects involve every drug in this class. (
  • The knowledge of all potential adverse effects is important and indeed time-sensitive, for physicians and patients both need complete information about risks and benefits to properly use COX-2 inhibitors and other clinical treatments. (
  • L'étude portait sur 20 patients atteints d'un carcinome gastrique, 20 patients souffrant d'une gastrite à H. pylori et 20 personnes en tant que groupe témoin. (
  • Because alternatives to the use of rifampin for antituberculosis treatment are now available, the previously recommended practice of stopping protease inhibitor therapy to allow the use of rifampin for TB treatment is no longer recommended for patients with HIV-related TB. (
  • However, the results did not show adverse effects of other COX-2 inhibitors on renal events and arrhythmia, indicating no overall evidence for a COX-2 inhibitor class effect. (
  • COX-1 "predominates in vascular smooth muscle and collecting ducts, whereas COX2 predominates in the macula densa and nearby cells in the cortical thick ascending limb" [ 2 ]. (
  • Ketorolac is a non-selective COX inhibitor of COX-1 and COX-2 with IC50 of 1.23 μM and 3.50 μM, respectively. (
  • Anti-cancer potency of cyclooxygenase inhibitors is established, but the mechanism of Cox-2-dependent potentiation of tumor growth is a subject of intense discussion. (
  • Results obtained in a panel of prostate cancer cell lines clearly indicate that cannabidiol is a potent inhibitor of cancer cell growth, with significantly lower potency in non-cancer cells. (
  • When coupled with cox-2 inhibitors the morphine not only provided better analgesic effects (better pain control), but also decreased the morbidity rate as welll as decreasing tumor growth rate. (
  • According to a recent online article published October 30, 207 in the British Journal of cancer, there might be a new use for the cox-2 inhibitors, in the treatment of cancer. (
  • Blanke, C 2004, ' Role of COX-2 inhibitors in cancer therapy ', Cancer Investigation , vol. 22, no. 2, pp. 271-282. (
  • OBJECTIVES: To evaluate the expression of COX-2 and HER2 and determine their correlation with clinicopathologic parameters in surgically resected histologically diagnosed cases of colorectal cancer. (
  • CONCLUSION: This study detects a high COX-2 and low HER2 expression in colorectal cancer using immunohistochemistry,suggesting a possible role for COX-2 in CRC pathogenesis.This report should trigger further investigations of both markers vis-à-vis the management of CRC in our environment. (
  • While COX-1 is mostly good for the body and protects the digestive tract, COX-2 is a contributing factor to arthritis, cancer, and Alzheimer's. (
  • When taken as directed, Mobic and Meloxicam generic works as a non-selective cyclooxygenase (COX) inhibitor. (
  • 3-Hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins) effectively reduce cholesterol levels and decrease the incidence of cardiovascular and cerebrovascular events (4). (
  • Proton pump inhibitors can control esophageal reflux symptoms. (
  • Such flames were fanned by two high-profile events last year: Eliot Spitzer's lawsuit against GlaxoSmithKline ( GSK ) for allegedly suppressing data linking antidepressants to suicide risk in children (which later prompted initiatives to disclose clinical trial results) and the recent scare over the safety of COX-2 inhibitors, a class of pain-killers, following the withdrawal by Merck of one of these called Vioxx. (
  • The role of Phosphodiesterase-1 and its natural product inhibitors in Alzheimer's disease: A review. (