Abstract
Two isoforms of cyclooxygenase (COX) are described: COX-1 is a constitutive enzyme and is widely expressed in most tissues, COX-2 is an inducible enzyme and is abundant throughout the gastrointestinal tract. Expression of COX-2 can be induced locally by inflammatory stimuli and appears coincident with local prostaglandin (PG) production. Currently available non-steroidal antiinflammatory drugs (NSAIDs) are widely used for the treatment of inflammatory diseases; however, significant side-effects due to inhibition of COX-1 limit their use. Inhibitors of COX-2 are as active as non-selective NSAIDs and inhibit PG synthesis in inflammatory cells. In contrast to other NSAIDs, selective COX-2 inhibitors do not cause ulcers in the stomach or intestine.
MeSH terms
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Animals
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Anti-Inflammatory Agents, Non-Steroidal / adverse effects*
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Cyclooxygenase 1
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Cyclooxygenase 2
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Cyclooxygenase 2 Inhibitors
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Cyclooxygenase Inhibitors / adverse effects*
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Humans
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Isoenzymes / physiology
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Membrane Proteins
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Nitrobenzenes / adverse effects
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Peptic Ulcer / chemically induced*
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Peroxidases / physiology
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Prostaglandin-Endoperoxide Synthases / physiology
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Pyrazoles / adverse effects
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Sulfonamides / adverse effects
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Thiophenes / adverse effects
Substances
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Anti-Inflammatory Agents, Non-Steroidal
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Cyclooxygenase 2 Inhibitors
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Cyclooxygenase Inhibitors
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Isoenzymes
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Membrane Proteins
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Nitrobenzenes
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Pyrazoles
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Sulfonamides
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Thiophenes
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N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide
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1-((4-methylsulfonyl)phenyl)-3-trifluoromethyl-5-(4-fluorophenyl)pyrazole
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DuP 697
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Peroxidases
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Cyclooxygenase 1
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Cyclooxygenase 2
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PTGS1 protein, human
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PTGS2 protein, human
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Prostaglandin-Endoperoxide Synthases