Prostaglandin-endoperoxide synthase (PTGS), also known as cyclooxygenase, is the key enzyme in prostaglandin biosynthesis, and acts both as a dioxygenase and as a peroxidase. There are two isozymes of PTGS: a constitutive PTGS1 and an inducible PTGS2, which differ in their regulation of expression and tissue distribution. This gene encodes the inducible isozyme. It is regulated by specific stimulatory events, suggesting that it is responsible for the prostanoid biosynthesis involved in inflammation and mitogenesis. [provided by RefSeq, Feb 2009 ...
TY - JOUR. T1 - Store-operated Ca2+ Entry Facilitates the Lipopolysaccharide-induced Cyclooxygenase-2 Expression in Gastric Cancer Cells. AU - Wong, Jhen Hong. AU - Ho, Kuo Hao. AU - Nam, Sean. AU - Hsu, Wen Li. AU - Lin, Chia Hsien. AU - Chang, Che Mai. AU - Wang, Jaw Yuan. AU - Chang, Wei Chiao. PY - 2017/12/1. Y1 - 2017/12/1. N2 - Helicobacter pylori has been identified as one of the major causes of chronic gastritis, gastric and duodenal ulcers, and gastric cancer. Lipopolysaccharide (LPS) is a major component of the outer membrane of gram-negative bacteria, and H. pylori LPS might play an exclusively important role in activating inflammatory pathways in monocytes and macrophages. To study the role of LPS in the underlying mechanism of inflammatory responses, we established an in vitro model using the human AGS gastric cancer cell line. We found that LPS mediates inflammation through setting off a cascade of events: activation of the store-operated calcium (SOC) channel, initiation of ...
PTGS2 (COX-2) is unexpressed under normal conditions in most cells, but elevated levels are found during inflammation. PTGS1 (COX-1) is constitutively expressed in many tissues and is the predominant form in gastric mucosa and in the kidneys. Inhibition of PTGS1 (COX-1) reduces the basal production of cytoprotective PGE2 and PGI2 in the stomach, which may contribute to gastric ulceration. Since PTGS2 (COX-2) is generally expressed only in cells where prostaglandins are upregulated (e.g., during inflammation), drug-candidates that selectively inhibit PTGS2 (COX-2) were suspected to show fewer side-effects[25] but proved to substantially increase risk for cardiovascular events such as heart attack and stroke. Two different mechanisms may explain contradictory effects. Low-dose aspirin protects against heart attacks and strokes by blocking PTGS1 (COX-1) from forming a prostaglandin called thromboxane A2. It sticks platelets together and promotes clotting; inhibiting this helps prevent heart ...
The size of the PCR products from cyclooxygenase-1 and cyclooxygenase-2 are 524 and 583 base pairs, respectively. The specificity of the PCR reaction for cyclooxygenase-1 and cyclooxygenase-2 complementary deoxyribonucleic acid (cDNA) was confirmed by digestion of PCR products by sequence-specific restriction enzymes (cyclooxygenase-1: Sac I and Sma I; cyclooxygenase-2: Pst I and Nco I). For quantitation of cyclooxygenase-1 and cyclooxygenase-2 mRNA levels, the Escherichia coli plasmid pT2M containing specific internal standards for cyclooxygenase-1 and cyclooxygenase-2 was constructed by internal deletion of sequences: The truncated fragments (320 base pairs) from cyclooxygenase-1 and cyclooxygenase-2 PCR products were incorporated into the E. coli cloning plasmid pBSII SK(+)(Stratagene, La Jolla, CA) at the EcoR I and Kpn I restriction sites and multiplied as plasmids in an E. coli strain Dh5 alpha. Plasmid solutions were adjusted to 1 x 104molecules/micro liter after double digestion by ...
bom:102287995 K00509 prostaglandin-endoperoxide synthase 1 [EC:1.14.99.1] , (RefSeq) PTGS1; prostaglandin-endoperoxide synthase 1 (A) MSRQGISLRFPLLLLLLSPSPVLPADPGAPAPVNPCCYYPCQHQGICVRFGLDRYQCDCT RTGYSGPNCTIPEIWTWLRTTLRPSPSFVHFLLTHGRWLWDFVNATFIRDTLMRLVLTVR SNLIPSPPTYNIAHDYISWESFSNVSYYTRILPSVPRDCPTPMGTKGKKQLPDAEFLSRR FLLRRKFIPDPQGTNLMFAFFAQHFTHQFFKTSGKMGPGFTKALGHGVDLGHIYGDNLER QYQLRLFKDGKLKYQMLNGEVYPPSVEEAPVLMHYPRGIPPQSQMAVGQEVFGLLPGLML YATIWLREHNRVCDLLKAEHPTWGDEQLFQTARLILIGETIKIVIEEYVQQLSGYFLQLK FDPELLFGAQFQYRNRIAMEFNQLYHWHPLMPDSFRVGPQDYSYEQFLFNTSMLVDYGVE ALVDAFSRQPAGRIGGGRNIDHHILHVAVDVIKESRELRLQPFNEYRKRFGMKPYTSFQE LTGEKEMAAELEELYGDINALEFYLGLLLEKCHPNSIFGESMIEMGAPFSLKGLLGNPIC SPEYWKASTFGGDVGFNLVKTATLKKLVCLNTKTCPYVSFHVPDPHREDRPGVERPPTEL ...
bom:102271174 K11987 prostaglandin-endoperoxide synthase 2 [EC:1.14.99.1] , (RefSeq) PTGS2; prostaglandin-endoperoxide synthase 2 (A) MLARALLLCAAVALSGAANPCCSHPCQNRGVCMSVGFDQYKCDCTRTGFYGENCTTPEFL TRIKLLLKPTPNTVHYILTHFKGVWNIVNKISFLRNMIMRYVLTSRSHLIESPPTYNVHY SYKSWEAFSNLSYYTRALPPVPDDCPTPMGVKGRKELPDSKEVVKKVLLRRKFIPDPQGT NLMFAFFAQHFTHQFFKTDFERGPAFTKGKNHGVDLSHIYGESLERQHKLRLFKDGKMKY QMINGEMYPPTVKDTQVEMIYPPHVPEHLKFAVGQEVFGLVPGLMMYATIWLREHNRVCD VLKQEHPEWGDEQLFQTSRLILIGETIKIVIEDYVQHLSGYHFKLKFDPELLFNQQFQYQ NRIAAEFNTLYHWHPLLPDVFQIDGQEYNYQQFIYNNSVLLEHGLTQFVESFTRQRAGRV AGGRNLPVAVEKVSKASIDQSREMKYQSFNEYRKRFLLKPYESFEELTGEKEMAAELEAL YGDIDAMEFYPALLVEKPRPDAIFGETMVEAGAPFSLKGLMGNPICSPEYWKPSTFGGEV GFKIINTASIQSLICSNVKGCPFTSFSVQDTHLTKTVTINASSSHSGLDDINPTVLLKER STEL ...
Cyclooxygenase (COX), officially known as prostaglandin-endoperoxide synthase (PTGS), is an enzyme that is responsible for formation of important biological mediators called prostanoids, including prostaglandins, prostacyclin and thromboxane. Pharmacological inhibition of COX can provide relief from the symptoms of inflammation and pain. Drugs, like Aspirin, that inhibit cyclooxygenase activity have been available to the public for about 100 years. Two cyclooxygenase isoforms have been identified and are referred to as COX-1 and COX-2. Under many circumstances the COX-1 enzyme is produced constitutively (i.e., gastric mucosa) whereas COX-2 is inducible (i.e., sites of inflammation). Non-steroidal anti-inflammatory drugs (NSAID), such as aspirin and ibuprofen, exert their effects through inhibition of COX. The main COX inhibitors are the non-steroidal anti-inflammatory drugs (NSAIDs).. ...
PTGS2 is the inducible isozyme of prostaglandin-endoperoxide synthase, also known as cyclooxygenase. It has been linked to numerous conditions, especially involving inflammation or cancer. Also known as COX2. [PMID 17479405] Haplotypes A-1195G-765T8473 and A-1195C-765T8473 variants of COX-2 were associated with 1.3X increased risk of breast cancer in a Chinese population [PMID 16361272] Relative to individuals with a PTGS2 Ex10 +837 TT genotype, those carrying the C allele (TC or CC genotype) had a 1.8-fold risk of bile duct cancer in a Chinese population [PMID 12920574] In a group of Pima Indians, individuals with the variant PTGS2 rs20417 CC genotype had a 30% higher Type 2 diabetes prevalence compared with subjects with the GG genotype ...
Cystic fibrosis (CF) is one of the most common autosomal recessive diseases among Caucasians caused by a mutation in the CFTR gene. However, the clinical outcome of CF pulmonary disease varies remarkably even in patients with the same CFTR genotype. This has led to a search for genetic modifiers located outside the CFTR gene. The aim of this study was to evaluate the effect of functional variants in prostaglandin-endoperoxide synthase genes (COX1 and COX2) on the severity of lung disease in CF patients. To the best of our knowledge, it is the first time when analysis of COX1 and COX2 as potential CF modifiers is provided. The study included 94 CF patients homozygous for F508del mutation of CFTR. To compare their clinical condition, several parameters were recorded, e.g. a unique clinical score: disease severity status (DSS). To analyse the effect of non-CFTR genetic polymorphisms on the clinical course of CF patients, the whole coding region of COX1 and selected COX2 polymorphisms were analysed. ...
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 the key enzyme in the biosynthetic pathway of prostaglandins (PGs) and thromboxane from arachidonic acid. There are two isozymes of cyclooxygenase; constitutive cyclooxygenase-1 and...
Cyclooxygenase is an enzyme that produces signals that can lead to pain and inflammation. Medications that inhibit cyclooxygenase...
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CONSTRUCTION AND OPTIMIZATION OF STRUCTURE-BASED VIRTUAL SCREENING PROTOCOLS TO IDENTIFY CYCLOOXYGENASE-1 INHIBITORS USING OPEN BABEL, SPORES AND PLANTS
高い抗原親和性、特異性と安定した品質を兼ね備えたアブカムのウサギ・モノクローナル抗体 RabMAb® ab62331 交差種: Ms,Hu 適用: WB,Flow Cyt,ICC/IF
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:1.14.99.1] ...
Sirtuin 1 (Sirt1) is a NAD+-dependent deacetylase that exerts many of the pleiotropic effects of oxidative metabolism. Due to local hypoxia and hypertonicity, the renal medulla is subject to extreme oxidative stress. Here, we set out to investigate the role of Sirt1 in the kidney. Our initial analysis indicated that it was abundantly expressed in mouse renal medullary interstitial cells in vivo. Knocking down Sirt1 expression in primary mouse renal medullary interstitial cells substantially reduced cellular resistance to oxidative stress, while pharmacologic Sirt1 activation using either resveratrol or SRT2183 improved cell survival in response to oxidative stress. The unilateral ureteral obstruction (UUO) model of kidney injury induced markedly more renal apoptosis and fibrosis in Sirt1+/¨C mice than in wild-type controls, while pharmacologic Sirt1 activation substantially attenuated apoptosis and fibrosis in wild-type mice. Moreover, Sirt1 deficiency attenuated oxidative stress¨Cinduced COX2 ...
Cyclooxygenase 1 (COX-1), also known as prostaglandin G/H synthase 1, prostaglandin-endoperoxide synthase 1 or prostaglandin H2 synthase 1, is an enzyme that in humans is encoded by the PTGS1 gene. In humans it is one of two cyclooxygenases. Cyclooxygenase (COX) is the central enzyme in the biosynthetic pathway to prostaglandins from arachidonic acid. This protein was purified more than 20 years ago and cloned in 1988. There are two isozymes of COX encoded by distinct gene products: a constitutive COX-1 (this enzyme) and an inducible COX-2, which differ in their regulation of expression and tissue distribution. The expression of these two transcripts is differentially regulated by relevant cytokines and growth factors. This gene encodes COX-1, which regulates angiogenesis in endothelial cells. COX-1 is also involved in cell signaling and maintaining tissue homeostasis. A splice variant of COX-1 termed COX-3 was identified in the CNS of dogs, but does not result in a functional protein in humans. ...
Non-steroidal anti-inflammatory drugs (NSAIDs), which include over-the-counter pharmaceuticals such as ibuprofen, naproxen, and aspirin, rank among the most widely used pharmaceuticals worldwide. Their chief mechanism of action is inhibition of two forms of cyclo-oxygenase (COX), namely COX-1 and COX-2 (1). Also known as prostaglandin-endoperoxide synthase (PTGS), COX is responsible for the production of downstream mediators of pain and inflammation, such as thromboxane and prostaglandins. Due to their suppression of prostaglandins, which exert protective roles in the gastrointestinal tract, one of the most frequent adverse effects of NSAIDs is irritation of the gastric mucosa.. Thus, newer generation selective COX-2 drugs, known as the coxibs, were introduced in the 1990s to mitigate the risk of peptic ulceration that results from COX-1 suppression. By 2004, coxibs had dominated the prescription drug market for NSAIDs, with worldwide sales of approximately $10 billion (2). Their development was ...
Ibuprofen is a well-established non-steroidal anti-inflammatory drug, inhibiting the prostaglandin-endoperoxide synthase. One of the key features defining the ibuprofen structure is the doubly intermolecular O-H⋯O [[double bond, length as m-dash]] C hydrogen bond in cyclic dimers as know from carboxylic acids a...
Cyclooxygenase (COX) is a bifunctional enzyme exhibiting coupled peroxidase and dioxygenase activities.1,2 Human COX-1 and COX-2 are two structurally homologous hemoproteins responsible for the biosynthesis of prostaglandin H2 from arachidonic acid (AA).1-3 They have been found to play great roles in certain diseases, including cancer,4 and nervous system5 and apoptosis-related diseases.6 COX-1 is constitutively expressed in a variety of cells,7 whereas COX-2 is induced by various inflammatory and proliferative stimuli. COX enzymes are important drug targets for the non-steroidal anti-inflammatory drugs. Over the past decades, COX-2 inhibitors have widely been used as anti-inflammatory medicine, although they usually elicit potential cardiotoxic side effects. Hence, many efforts have been made in recent years to eliminate or reduce such kinds of adverse effects.6,8,9 Crystal structure studies10,11 reveal that COX-2 has a larger substrate binding pocket than COX-1 (Fig. S1†), providing the ...
Coincident with the FDA approval of refecoxib and celecoxib, FitzGerald et al reported that these drugs suppress the formation of prostacyclin (PGI2), leaving the production of thromboxane A2 (TXA2) unaltered.30 PGI2 is a key COX product in the endothelium that inhibits platelet aggregation, causes vasodilatation, and prevents proliferation of vascular smooth muscle cells.31 Evidence was also provided that PGI2 production in vivo was COX-2 dependent, possibly through COX-2 induction in endothelial cells by shear stress.31 In contrast to PGI2, the COX-1-derived prostanoid TXA2, causes platelet aggregation, vasoconstriction, and vascular proliferation.31 FitzGerald et al speculated that suppression of COX-2-dependent formation of PGI2 by the COX-2 inhibitors left TXA2 generation unopposed, promoting vasoconstriction, thrombosis, and atherogenesis.32 A number of publications began to surface suggesting that the COX-2 inhibitors might be associated with an increased risk of cardiovascular events. ...
The role of NSAIDs in the prevention of colorectal cancer is mediated through various mechanisms including the inhibition of COX-2 and the induction of apoptosis through COX-2 independent pathways (26). Previous studies from our laboratory suggested that ASA partially suppresses the MSI-H phenotype of human colon cancer cell lines through an apoptotic mechanism that appeared to be COX independent (22). In vitro ASA has been shown to arrest colon cancer cells at the G1/S checkpoint and induce apoptosis through activation of ATM, p21, and BAX (27). Among NSAIDS, ASA is still a preferred choice for chemoprevention in average-risk individuals. This is not only because of its shown chemopreventive efficacy but also because of its unique potential in cardiovascular protection (3, 4).. In this study, we investigated the chemopreventive potential of ASA and NO-ASA using a newly developed mouse model of LS/HNPCC. LS/HNPCC mice treated with ASA at 400 mg/kg had an increased median survival time compared ...
Cyclooxygenase-2 (COX-2)-dependent prostaglandin E2 (PGE2) synthesis exacerbates occlusive and aneurysmal vascular disease by inducing macrophage proteinase and...
Sevigny M.B., Li C.F., Alas M., Hughes-Fulford M.. Cyclooxygenase-2 (COX-2) catalyzes the rate-limiting step in the prostanoid biosynthesis pathway, converting arachidonic acid into prostaglandin H(2). COX-2 exists as 72 and 74kDa glycoforms, the latter resulting from an additional oligosaccharide chain at residue Asn(580). In this study, Asn(580) was mutated to determine the biological significance of this variable glycosylation. COS-1 cells transfected with the mutant gene were unable to express the 74kDa glycoform and were found to accumulate more COX-2 protein and have five times greater COX-2 activity than cells expressing both glycoforms. Thus, COX-2 turnover appears to depend upon glycosylation of the 72kDa glycoform.. FEBS Lett. 580:6533-6536(2006) [PubMed] [Europe PMC] ...
Rabbit recombinant monoclonal COX2 / Cyclooxygenase 2 antibody [EPR18376-119] validated for WB, IP, Flow Cyt, ICC/IF and tested in Mouse. Immunogen…
So the problem has to do with the fact that sometimes our understanding of how the body does what it does is incomplete, and when we isolate a chemical or split a natural chemical down to only part of its molecule, it ends up turning off one bad function of the body but unwittingly turning off some beneficial functions, too. For instance, aspirin inhibits cyclooxygenase, the bodys natural chemical that normally mediates the synthesis of natural chemicals that enable platelets to activate and stick together and form a clot when blood vessel damage occurs so you dont bleed out... some people are inappropriately prone to clotting and need to tone that natural process down a bit, so they take aspirin. Well, unfortunately cyclooxygenase also mediates processes that cause your stomach to protect its lining against its own acid... so inhibiting cyclooxygenase will stop platelets of clot-prone people from clotting inappropriately, but at the same time it has the potential to also cause you to get a ...
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 ...
Drug Discovery, Drugs, Inflammation, Pain, Therapeutic, Community, Homo, Inhibition, Mechanics, Cyclooxygenase, Cyclooxygenase-1, Literature, Pathologies
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. ...
Background Giardia lamblia trophozoites colonize in the upper small intestine resulting in diarrhea and various clinical manifestations, including abdominal pain, anorexia, and signs of malabsorption. A decrease in the level of trace elements might occur because of this absorption deficiency resulting from giardiasis. Experimentally, the excretory secretory product of G. lamblia trophozoites increased the level of reactive oxygen species in mice enterocytes. The levels of bilirubin, uric acid, and albumin are often used as major nonenzymatic oxidative biomarkers. Objective This study was designed to determine the effect of therapy by metronidazole (MTZ) and artemether (ART) on trophozoite and cyst forms in experimentally Giardia spp.-infected hamsters and to reveal the changes in iron (Fe), manganese (Mn), copper (Cu), and chromium (Cr) serum levels pretreatment and post-treatment. Another objective was to evaluate the impact of this therapy on serum levels of bilirubin, uric acid, and albumin ...
We have recently reported that cyclooxygenase (COX)-2-deficiency affects brain upstream and downstream enzymes in the arachidonic acid (AA) metabolic pathway to prostaglandin E2 (PGE2), as well as enzyme activity, protein and mRNA levels of the reciprocal isozyme, COX-1. To gain a better insight into the specific roles of COX isoforms and characterize the interactions between upstream and downstream enzymes in brain AA cascade, we examined the expression and activity of COX-2 and phospholipase A2 enzymes (cPLA2 and sPLA2), as well as the expression of terminal prostaglandin E synthases (cPGES, mPGES-1, and − 2) in wild type and COX-1-/- mice. We found that brain PGE2 concentration was significantly increased, whereas thromboxane B2 (TXB2) concentration was decreased in COX-1-/- mice. There was a compensatory up-regulation of COX-2, accompanied by the activation of the NF-κB pathway, and also an increase in the upstream cPLA2 and sPLA2 enzymes. The mechanism of NF-κB activation in the ...
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This invention is in the field of antiinflammatory pharmaceutical agents and specifically relates to compounds, compositions and methods for treating disorders mediated by cyclooxygenase-2 or 5-lipoxygenase, such as inflammation. Compounds of particular interest are defined by Formula I wherein A, Y, R1, R2, R3, R4 and R5 are as defined in the specification.
COX-1抑制劑篩選K548 | COX活性測定試劑盒 | COX-2抑制劑篩選試劑盒 | 環氧合酶2(COX-2)ELISA試劑盒 | PTGS2 / COX-2(人類)ELISA試劑 COX-1抑制劑篩選試劑盒 | 貨號K548 Cyclooxygenase-1 (COX-1) Inhibitor
Liu, X., Wong, P.T.-H., Lee, T.L. (2006). Cyclooxygenase-1 inhibition shortens the duration of diazepam-induced loss of righting reflex in mice. Anesthesia and Analgesia 102 (1) : 135-140. [email protected] Repository. https://doi.org/10.1213/01.ane.0000189102.09347. ...
Eicosanoids exert their cellular action through specific G-protein coupled receptors. Prostanoids are the products of cyclooxygenases action on C-20…
p,Hyperproduced prostaglandin E,sub,2,/sub, by cyclooxygenase-2 and microsomal prostaglandin E synthase-1 evokes several pathophysiological responses such as inflammation and carcinogenesis. Our recent study demonstrated that ,i,Dioscorea japonica,/i, extract suppressed the expression of cyclooxygenase-2 and microsomal prostaglandin E synthase-1 and induced apoptosis in lung carcinoma A549 cells. In the present study, we investigated the effects of ,i,Dioscorea japonica,/i, on squamous cell carcinoma of mouse skin. ,i,Dioscorea japonica,/i, feeding and ,i,Dioscorea japonica,/i, extract topical application suppressed the expression of cyclooxygenase-2, microsomal prostaglandin E synthase-1, interleukin-1β and interleukin-6 and inhibited tumor formation, hyperplasia and inflammatory cell infiltration. Immunohistochemical analyses showed the immunoreactivities of cyclooxygenase-2 and microsomal prostaglandin E synthase-1 in tumor keratinocytes and stronger immunoreactivities of cyclooxygenase-2 ...
hypothetical protein, gbf1, Anapl_04335, AS27_01565, AS28_01193, C79137, C9orf15, CB1_000576027, D623_10025025, gamma-interferon-activated transcriptional element-binding factor 1, GATE-binding factor 1, GBF-1, H920_19196, I79_014770, M91_12705, M959_12051, MDA_GLEAN10019304, membrane-associated prostaglandin E synthase 2, membrane-associated prostaglandin E synthase-2, microsomal prostaglandin E synthase 2, microsomal prostaglandin E synthase-2, Mpges2, MPGES-2, mPGE synthase-2, N300_09271, N301_12743, N302_13172, N303_06092, N305_09010, N306_14810, N307_02442, N308_10508, N311_11677, N312_00533, N320_07005, N321_11509, N322_00413, N324_09565, N325_00199, N326_00389, N327_11175, N328_09700, N329_10988, N330_00570, N331_03110, N332_07603, N333_00239, N334_00603, N335_09322, N336_03658, N339_06101, N340_07113, N341_11017, PAL_GLEAN10012478, PANDA_003194, pges2, prostaglandin E receptor 2, prostaglandin E synthase 2-like protein, prostaglandin-H(2) E-isomerase, TREES_T100004307, UY3_04702, ...
Accepted name: prostaglandin-endoperoxide synthase. Reaction: arachidonate + reduced acceptor + 2 O2 = prostaglandin H2 + acceptor + H2O. Other name(s): prostaglandin synthase; prostaglandin G/H synthase; (PG)H synthase; PG synthetase; prostaglandin synthetase; fatty acid cyclooxygenase; prostaglandin endoperoxide synthetase. Systematic name: (5Z,8Z,11Z,14Z)-icosa-5,8,11,14-tetraenoate,hydrogen-donor:oxygen oxidoreductase. Comments: This enzyme acts both as a dioxygenase and as a peroxidase.. Links to other databases: BRENDA, EXPASY, KEGG, Metacyc, PDB, CAS registry number: 39391-18-9. References:. 1. DeWitt, D.L. and Smith, W.L. Primary structure of prostaglandin G/H synthase from sheep vesicular gland determined from the complementary DNA sequence. Proc. Natl. Acad. Sci. USA 85 (1988) 1412-1416. [PMID: 3125548]. 2. Ohki, S., Ogino, N., Yamamoto, S. and Hayaishi, O. Prostaglandin hydroperoxidase, an integral part of prostaglandin endoperoxide synthetase from bovine vesicular gland microsomes. ...
The potential role of arachidonic acid metabolism in the enhancement (promotion) of malignant transformation of C3H/M2 mouse fibroblasts by the tumor promoter 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) was investigated using inhibitors of cyclooxygenase and lipoxygenase activities. The promoting effects of TCDD (1.5 pM) and of the reference tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA; 0.4 mM) on carcinogen (N-methyl-N′-nitro-N-nitrosoguanidine or 3-methylcholanthrene)-pre-treated fibroblasts was abolished by cotreatment with indomethacin, hydrocortisone, caffeic acid or nordihydroguaiaretic acid. A differential inhibition was found with N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide, a selective inhibitor of the cyclooxygenase isoenzyme COX-2: the promoting effect of TPA, but not that of TCDD, was abolished. Therefore, the role of the cyclooxygenase isoenzymes COX-1 and COX-2 during chronic exposure to TCDD was studied in more detail. Long-term treatment with TCDD (4-7 weeks) ...
Inflammation comprises the reaction of the body to injury, in which a series of changes of the terminal vascular bed, blood, and connective tissue tends to eliminate the injurious agent and to repair the damaged tissue. It is a complex process, which involves the release of diverse regulatory mediators. The current anti-inflammatory agents are challenged by multiple side effects and thus, new effective therapies are highly needed. The aim of this review is to summarize the described microsomal prostaglandin E synthase-1 (mPGES-1) inhibitors or transcriptional suppressors from medicinal plants, which could be an ideal approach in the management of inflammatory disorders, but need further clinical trials in order to be ultimately validated ...
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 ...
Cyclooxygenase 2 (COX-2) is a key enzyme in the transformation of arachidonic acidity to prostaglandins and COX-2 overexpression has an important function in carcinogenesis. modulation of USF transcriptional activity in the 5? upstream area from the COX-2 gene. Right here we discovered that apigenin treatment also elevated COX-2 mRNA balance as well as the inhibitory aftereffect of apigenin on UVB-induced luciferase reporter gene activity was reliant on the Saxagliptin AU-rich component of the COX-2 3?-untranslated area. Furthermore we discovered two RNA-binding protein HuR as well as the T-cell-restricted intracellular antigen 1-related proteins (TIAR) that have been connected with endogenous COX-2 mRNA in 308 keratinocytes and apigenin treatment elevated their localization to cell cytoplasm. Moreover Saxagliptin reduced amount of HuR amounts by little interfering RNA inhibited apigenin-mediated stabilization of COX-2 mRNA. Cells expressing decreased TIAR showed proclaimed level of resistance ...
The widespread consumption of diets rich in anthocyanin and catechin content prompted the evaluation of their in vitro inhibitory effects on cyclooxygenase (COX) enzymes and on the proliferation .... ...
N-(3,4-dichlorobiphenyl-4-yl)-4-hydroxy-2H-1,2-benzothiazine-3-carboxamide 1,1-dioxide: a microsomal prostaglandin E synthase-1 inhibitor; structure in first source
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 ...
Abstract The effect of water extracts of doenjang (WED) on cyclooxygenase pathway and cytokine production in lipopolysaccharide (LPS)-treated RAW 264.7 macrophage cells was investigated. WED was fractionated by ultrafiltration into five individual groups of molecular weights. All of the WED fractions significantly inhibited the production of prostaglandin E2 (PGE2) and expression of cyclooxygenase-2 (COX-2) in LPS-stimulated RAW 264.7 macrophages. Furthermore, each of the WED fractions significantly decreased production of pro-inflammatory cytokine such as tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) (p,0.05). The fraction between 10 to 30 kDa of WED showed the highest inhibition of pro-inflammatory cytokine production, LPS-induced COX-2 ...
Introduction New fluorinated diaryl ethers and bisarylic ketones were designed and evaluated for their anti-inflammatory effects in primary macrophages. Methods The synthesis of the designed molecules started from easily accessible and versatile gem-difluoro propargylic derivatives. The desired aromatic systems were obtained using Diels-Alder/aromatization sequences and this was followed by Pd-catalyzed coupling reactions and, when required, final functionalization steps. Both direct inhibitory effects on cyclooxygenase-1 or -2 activities, protein expression of cyclooxygenase-2 and nitric oxide synthase-II and the production of prostaglandin E-2, the pro-inflammatory nitric oxide and interleukin-6 were evaluated in primary murine bone marrow-derived macrophages in response to lipopolysaccharide. Docking of the designed molecules in cyclooxygenase-1 or -2 was performed. Results Only fluorinated compounds exerted anti-inflammatory activities by lowering the secretion of interleukin-6, nitric oxide, and