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Cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) are key enzymes responsible for the conversion of arachidonic acid to prostaglandins in the gastric mucosa; COX-1 is constitutively expressed and mediates baseline protective prostaglandin production, while COX-2 is inducible during inflammation. Prostaglandins synthesized in the gastric mucosa are essential for maintaining mucosal integrity, regulating acid secretion, and promoting epithelial cell restitution. Inhibition of COX enzymes, particularly by nonsteroidal anti-inflammatory drugs (NSAIDs), reduces mucosal prostaglandin synthesis and increases susceptibility to gastric injury and ulceration. Conversely, prostaglandin analogs such as misoprostol can supplement protective prostaglandins and are used clinically to prevent NSAID-induced ulcers.
Inhibition of cyclooxygenase activity, reducing prostaglandin synthesis (nonselective and selective NSAIDs); Mimicry or supplementation of prostaglandins (e.g., misoprostol)
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