The gastric mucosa produces prostaglandins E2 (PGE2) and prostacyclin (PGI2), crucial in maintaining gastric health. They exert cytoprotective effects, including increasing bicarbonate secretion, releasing protective mucin, reducing gastric acid output, and preventing harmful vasoconstriction. These effects are mediated through various receptors, such as EP1, EP2, EP3, and EP4.

Non-steroidal anti-inflammatory drugs (NSAIDs) can induce peptic ulcers by inhibiting cyclooxygenase, decreasing prostaglandin production. This deficiency, particularly in PGE2 and PGI2, contributes to ulcer formation by disrupting the protective mechanisms of the gastric mucosa.

Misoprostol, a synthetic analog of prostaglandin E1, is used to counteract these adverse effects. It inhibits basal gastric acid secretion and acid production in response to food, pentagastrin, and caffeine. Additionally, it increases mucosal blood flow and enhances mucus and bicarbonate secretion, preventing gastric damage from chronic NSAID use.

Clinically, misoprostol is used for ulcer prevention, especially in high-risk patients. However, its usage is limited due to clinical exacerbations of inflammatory bowel disease and adverse effects like diarrhea, abdominal cramps, uterine contractions, and therefore, contraindicated in pregnant women.