INT73599
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Whereas paracetamol inhibited only COX enzyme activity, caffeine also inhibited COX-2 protein synthesis. | |||||||||||||||
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Sodium valproate, a mood stabilizer, when chronically administered to rats (200 mg/kg i.p. daily for 30 days) significantly reduced the brain protein levels of cyclooxygenase (COX)-1 and COX-2, without altering the mRNA levels of these enzymes. | |||||||||||||||
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NSAIDs, retinoids, antioxidants, and PPAR agonists, reported to be chemopreventive, suppress COX-2 synthesis. | |||||||||||||||
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Evidence suggests that nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit cycloxygenase (COX) and production of the proinflammatory prostaglandin, PGE2, and thus prevent carcinogenesis in the colon. | |||||||||||||||
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Dexamethasone treatment reduced the expression of both COX-2 and PGEs in kainate-treated animals. | |||||||||||||||
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Moreover, ethanol fractions potently suppressed the expression of cycloxygenase (COX)-2 and granulocyte-macrophage colony-stimulating factor (GM-CSF), which are stimulated by LPS in RAW264.7 cells. | |||||||||||||||
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Although COX-1 mRNA was expressed in the colon without much alteration during the test period, the expression of COX-2 was upregulated with a peak on day 3 and decreased thereafter. | |||||||||||||||
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Yet all these agents inhibited not only the bacterial invasion but also the expression of COX-2 and iNOS activity in the intestinal mucosa following indomethacin treatment, resulting in the prevention of intestinal lesions. | |||||||||||||||
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The data also showed that NF-kappaB activation and its associated gene expressions, such as COX-2, iNOS, VCAM-1 and ICAM-1, were all suppressed by the low dose aspirin supplementation through the inhibition of phosphorylation and degradation of IkappaBalpha via the NIK/IKK pathway. | |||||||||||||||
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By contrast, we found that LAE (0.02 microg/ml) selectively inhibited prostaglandin E2 production by cyclooxygenase (COX)-2, but not COX-1, which is a plausible mechanism for the analgesic effect. | |||||||||||||||
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Non-steroidal anti-inflammatory drugs (NSAIDs) are thought to exert their pharmacological actions by a common mechanism: inhibition of cyclooxygenase (COX)-mediated prostanoid synthesis. | |||||||||||||||
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High-dose flosulide treatment reduced renal prostaglandin production and caused a marked decline in COX-1 and COX-2 protein expression. | |||||||||||||||
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Resveratrol also prevented the bilateralisation of COX-2 expression. | |||||||||||||||
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By contrast, we found that LAE (0.02 microg/ml) selectively inhibited prostaglandin E2 production by cyclooxygenase (COX)-2, but not COX-1, which is a plausible mechanism for the analgesic effect. | |||||||||||||||
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The intestinal hypermotility caused by COX-1 inhibition may be a key to COX-2 expression after administration of NSAIDs and their intestinal ulcerogenic properties.
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The expression of cyclooxygenase (COX)-1, COX-2, and inducible nitric oxide synthase (iNOS) was inhibited by 2 Hz EA in carrageenan-injected rat paws. | |||||||||||||||
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Evaluation of 5-LOX metabolites-by LC/MS/MS and ELISA confirmed that both compounds selectively inhibited all products downstream of 5-hydroperoxy eicosatetraenoic acid (5-HPETE), including 5-oxo-6,8,11,14-eicosatetraenoic acid (5-oxoETE), without inhibition of 12-lipoxygenase (12-LOX), 15-lipoxygenase (15-LOX), or cyclooxygenase (COX) products. | |||||||||||||||
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Nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit cyclooxygenase (COX) activity and the local production of COX products that affect inflammation [1]. | |||||||||||||||
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The expression of cyclooxygenase (COX)-1, COX-2, and inducible nitric oxide synthase (iNOS) was inhibited by 2 Hz EA in carrageenan-injected rat paws. | |||||||||||||||
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COX-1 expression in cortical collecting tubules was significantly reduced in G3 and G4 compared with G1 and G2 (P < 0.05 for all). | |||||||||||||||
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General Comments
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