Prostaglandin

Prostaglandins are a group of physiologically active lipid compounds that belong to the eicosanoid family. They are derived from arachidonic acid and synthesized on demand in nearly all tissues. Prostaglandins act as local hormones, exerting paracrine and autocrine effects with rapid onset and short duration of action.

Biosynthesis occurs when phospholipase A2 releases arachidonic acid from membrane phospholipids. Cyclooxygenases (COX-1 and COX-2) convert it to prostaglandin H2, a common precursor that is further converted by specific synthases into distinct prostaglandins, including PGE2, PGD2, PGF2alpha, and prostacyclin (PGI2). Thromboxane A2 (TXA2) is a related COX-derived mediator produced mainly by platelets and promotes platelet aggregation and vasoconstriction. Prostaglandins exert their effects by binding to G protein–coupled receptors (for example, PGE2 to EP1–EP4 receptors; PGD2 to DP receptors; PGF2alpha to FP; PGI2 to IP; TXA2 to TP).

Physiological roles are diverse. Prostaglandins participate in inflammation, fever, and pain modulation; regulate vascular tone and renal function; protect gastric mucosa; and influence airway tone and labor by affecting uterine smooth muscle. In the reproductive system, PGE2 and PGF2alpha help control cervical ripening and uterine contractions.

Clinical relevance includes the use of nonsteroidal anti-inflammatory drugs (NSAIDs) that inhibit COX and reduce prostaglandin synthesis. Therapeutic prostaglandin analogs and antagonists are used for various indications: misoprostol (PGE1) for gastric protection and abortion adjuncts; dinoprostone (PGE2) for cervical ripening; alprostadil (PGE1) to maintain ductus arteriosus and treat erectile dysfunction; prostacyclin analogs (epoprostenol, iloprost, treprostinil) for pulmonary arterial hypertension; and prostaglandin F2alpha analogs (latanoprost, travoprost) for glaucoma. Prostaglandins are rapidly inactivated and not stored in tissues, reflecting their tightly regulated, locally acting nature.