Gastric mucosal prostaglandin synthesis pathway

The gastric mucosal prostaglandin synthesis pathway is a fundamental physiological system that maintains the structural and functional integrity of the stomach lining against aggressive factors like gastric acid and pepsin. This pathway involves the enzymatic conversion of arachidonic acid into bioactive prostanoids, primarily prostaglandin E2 (PGE2) and prostacyclin (PGI2), mediated by cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) [1][2]. These prostaglandins exert "cytoprotective" effects by stimulating the production of a protective mucus-bicarbonate barrier, promoting mucosal blood flow to remove back-diffused acid, and directly inhibiting acid secretion from parietal cells via EP3 receptors [3][4]. Clinical relevance of this pathway is most prominent in the context of nonsteroidal anti-inflammatory drugs (NSAIDs), which inhibit COX enzymes and deplete gastric prostaglandins, often leading to gastritis and peptic ulceration [1][5]. Therapeutic strategies targeting this pathway include the use of synthetic prostaglandin analogs, such as misoprostol, to restore mucosal defenses, or the development of COX-2 selective inhibitors to minimize gastrointestinal toxicity [2][6].

Other names

Gastric prostaglandin pathwayCyclooxygenase pathway in the stomachGastric cytoprotective pathwayArachidonic acid metabolism in gastric mucosa

Inhibition of cyclooxygenase enzymes (COX-1 and COX-2) reduces the synthesis of protective prostaglandins (PGE2 and PGI2), while prostaglandin analogs act as agonists at EP receptors to restore cytoprotection.