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The inhibition of COX-2 is mostly responsible for the
therapeutic effects of NSAIDs, while the adverse gastrointestinal
(GI) effects of NSAIDs are attributable to the
inhibition of both COX-1 and COX-2, which decreases
prostaglandin synthesis, impairs the maintenance of GI
mucosal integrity, and results in erosion, ulceration, and
bleeding [3,4]. Coxibs selectively inhibit COX-2 and thus
inhibit inflammation while preserving most of the homeostatic
functions of COX-derived prostaglan
The inhibition of COX-2 is mostly responsible for the
therapeutic effects of NSAIDs, while the adverse gastrointestinal
(GI) effects of NSAIDs are attributable to the
inhibition of both COX-1 and COX-2, which decreases
prostaglandin synthesis, impairs the maintenance of GI
mucosal integrity, and results in erosion, ulceration, and
bleeding [3,4]. Coxibs selectively inhibit COX-2 and thus
inhibit inflammation while preserving most of the homeostatic
functions of COX-derived prostaglan
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