INT76427
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
The aim of this study was to investigate the role of cyclooxygenase (COX) inhibition in intestinal motility and in the extent of tissue injury of the small intestine and liver with the use of various COX inhibitors. | |||||||||||||||
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Since the discovery of at least two isozymes of cyclooxygenase (COX), inhibition of COX-2 has been suggested to be responsible for the therapeutic effects of nonsteroidal anti-inflammatory drugs (NSAIDs). | |||||||||||||||
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To assess the mechanism of action of a COX-2 inhibitor, we studied the expression of COX-2 and assayed plasma levels of prostaglandins, and also compared the clinical effect of a COX-2 inhibitor with a 5-lipoxygenase (LO) inhibitor, which is responsible for another pathway of arachidonic acid metabolism. | |||||||||||||||
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We studied the influence of specific COX-2 inhibitors on this decrease of MAC. | |||||||||||||||
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A synergistic effect of nonselective cyclooxygenase (COX) inhibitors on morphine-induced decrease of isoflurane minimum alveolar concentration (MAC(ISO)) has been observed in the rat. | |||||||||||||||
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The effect of alpha-MSH on reactive oxygen species (ROS) production by rat peritoneal neutrophils and the effect of cyclooxygenase (COX) inhibition were investigated using the chemiluminescence (CL) technique. | |||||||||||||||
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Role of cyclooxygenase (COX)-1 and COX-2 inhibition in nonsteroidal anti-inflammatory drug-induced intestinal damage in rats: relation to various pathogenic events. | |||||||||||||||
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The changes in our view of the importance of NSAID-induced cyclo-oxygenase (COX) inhibition on the pathogenesis and prevention of NSAID-induced gastrointestinal injury is presented. | |||||||||||||||
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The aim of this study was to investigate the role of cyclooxygenase (COX) inhibition in intestinal motility and in the extent of tissue injury of the small intestine and liver with the use of various COX inhibitors. | |||||||||||||||
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This is supported by a previous study performed in LPS-stimulated human adult microglial cells, in which selective inhibition of COX-1 was also very effective in reducing PGE2 production [62]. | |||||||||||||||
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In this study, we examined the effects of various inhibitors of cyclooxygenase (COX) or NO synthase (NOS) on the acid-induced HCO3- secretion in rats and determined the enzyme isoforms responsible for this response. | |||||||||||||||
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This review discusses: 1) how two separate catalytic processes in COX - peroxidase and prostaglandin synthase - act in an integrated fashion manner to generate prostaglandins; 2) why irreversible inactivation of COX is important constitutively and pharmacologically; 3) how cells have managed to use two closely related, almost identical enzymes in ways that discriminate their physiological versus pathological roles; 4) how investigators have used these advances to formulate and test medically important uses for old drugs (i.e. aspirin) and create new ones that still seek to achieve Hoffman's original goal. | |||||||||||||||
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Studies have shown that both therapeutic and side effects of NSAIDs are dependent on cyclooxygenase (COX) inhibition. | |||||||||||||||
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Such critical adverse reactions are mostly dependent on COX-1 inhibition. | |||||||||||||||
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OBJECTIVE: To determine the effect of 3 different cyclo-oxygenase (COX) inhibitors on primary dysmenorrheic pain. | |||||||||||||||
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Anti-inflammatory effects of NSAIDs are mediated by COX-2 inhibition, while COX-1 inhibition is responsible for gastric prostaglandin inhibition. | |||||||||||||||
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It was found that their action is centred on the inhibition of the cyclooxygenase (COX) enzyme responsible for converting arachidonic acid to prostaglandins. | |||||||||||||||
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Several currently available nonsteroidal anti-inflammatory drugs (NSAIDs) have been evaluated for their relative selectivity in inhibiting the two cyclooxygenase (COX) isozymes, COX-1 and COX-2. | |||||||||||||||
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Nonspecific COX inhibition appears to be responsible for much of the toxicity of NSAIDs. | |||||||||||||||
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Role of COX inhibition in pathogenesis of NSAID-induced small intestinal damage. | |||||||||||||||
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