Prostaglandina

Prostaglandina, commonly referred to in English as prostaglandin, is part of the larger class of lipid compounds known as prostanoids, derived from arachidonic acid. They are produced by many cell types and function as local mediators rather than hormones that travel long distances. Biosynthesis begins with release of arachidonic acid from membrane phospholipids by phospholipase A2. Cyclooxygenases COX-1 and COX-2 convert arachidonic acid to prostaglandin G2 and subsequently to prostaglandin H2, which is then transformed by tissue-specific synthases into various active prostanoids, including PGE2, PGD2, PGF2α, and prostacyclin (PGI2).

Prostaglandins act through specific G protein–coupled receptors. PGE2 signals via EP receptors (EP1–EP4), PGD2 via DP receptors (DP1 and DP2/CRTH2), PGF2α via FP receptors, and PGI2 via IP receptors; TXA2 signals through TP receptors. These mediators regulate diverse physiological processes, including inflammation and pain, fever, vascular tone and permeability, gastric mucosal protection, renal blood flow, and platelet aggregation. In the reproductive system, PGF2α and PGE2 influence uterine contractions and cervical ripening.

Clinical relevance is broad. Nonsteroidal anti-inflammatory drugs inhibit COX enzymes to reduce prostaglandin synthesis. Analogues and derivatives have therapeutic roles: misoprostol (PGE1) to protect the stomach; dinoprostone (PGE2) for cervical ripening; alprostadil (PGE1) for maintaining ductus arteriosus or erectile dysfunction; prostaglandin analogs for glaucoma (eg, latanoprost) and for pulmonary arterial hypertension (epoprostenol). Prostaglandins are rapidly metabolized and act locally, with effects that are highly context- and tissue-dependent.