INT27964
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
The qualitative effects of zomepirac on platelets are assumed to be the consequence of reversible inhibition of prostaglandin synthetase in these cells. | |||||||||||||||
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However, the long-term use of anti-inflammatory drugs in the treatment in periodontal disease requires confirmation of experimental results in long-term prospective and independent trials in humans, and elucidation and control of possible side effects due to the inhibition of prostaglandin-sintetase. | |||||||||||||||
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Indomethacin is an effective inhibitor of prostaglandin synthetase and has recently been demonstrated to inhibit inflammatory fluid secretion into the gallbladder in experimental cholecystitis. | |||||||||||||||
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The inhibitory effects of some anti-inflammatory drugs on skin microsomal prostaglandin synthetase were also demonstrated in these studies. | |||||||||||||||
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Stereoselective inhibition of carbonyl reductase from rabbit kidney by enantiomers of carprofen. | |||||||||||||||
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Prostaglandin synthetase inhibitors, non-steroidal anti-inflammatory drugs, have been utilized for the past two decades in many animal studies, especially in endotoxin or septic shock, to determine what effects they might have. | |||||||||||||||
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Formation of M4 and M5 was catalyzed by NADPH-dependent hepatic cytosolic enzymes, which were identified using selective chemical inhibitors (10 and 100 microM) for aldo-keto reductase (AKR) isoforms, short-chain dehydrogenase/reductase including carbonyl reductase, alcohol dehydrogenase, and quinone oxidoreductase. | |||||||||||||||
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Since both indomethacin and diclofenac sodium are potent inhibitors of prostaglandin synthetase, these findings are consistent with the hypothesis tht prostaglandins are involved in the feed-back regulation of lipolysis, and mediate the inhibitory effect of lipolysis on lipoprotein lipase activity. | |||||||||||||||
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It is estimated that 10-30% of patients with painful periods fail to respond to prostaglandin (PG) synthetase inhibitors. | |||||||||||||||
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In a randomized double-blind trial, the effect of ibuprofen on the pain produced by gallbladder disease and on gallbladder mucosa and muscle wall tissue PGE and PGF production was evaluated to determine if the pain of cholecystitis and prostaglandin formation were altered by administration of a prostaglandin synthetase inhibitor. | |||||||||||||||
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Prostaglandin synthetase inhibition decreases the pain associated with cholecystitis; however, the absence of correlation with decreased PGE formation suggests that other prostanoids may play an important role in producing the symptoms of cholecystitis. | |||||||||||||||
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Non-steroidal anti-inflammatory drugs (NSAIDs) are known to inhibit prostaglandin synthetic enzyme, cyclooxygenases (COXs), as well as to exhibit anti-tumor activity although at much higher concentrations. 15-Hydroxyprostaglandin dehyrogenase (15-PGDH), a key prostaglandin catabolic enzyme, was recently shown to be a tumor suppressor. | |||||||||||||||
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General Comments
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