ProstaglandinH2

Prostaglandin H2 (PGH2) is a prostaglandin endoperoxide that serves as the central biosynthetic intermediate for the prostanoids. It is produced from arachidonic acid by the cyclooxygenase enzymes COX-1 and COX-2. COX first converts arachidonic acid to prostaglandin G2 (PGG2), and its peroxidase activity then reduces PGG2 to PGH2. PGH2 is an unstable, short‑lived molecule that functions primarily as a substrate for tissue-specific synthases that generate the downstream prostanoids.

PGH2 is converted by distinct synthases into several important mediators, including prostaglandin E2 (PGE2), prostaglandin D2 (PGD2), prostaglandin F2α (PGF2α), thromboxane A2 (TXA2), and prostacyclin (PGI2). The distribution of these synthases across cells and tissues determines local prostanoid profiles and influences inflammation, vascular tone, platelet aggregation, and mucosal protection.

As a common precursor, PGH2 provides a mechanistic link between COX activity and a broad range of physiological effects. Nonsteroidal anti-inflammatory drugs (NSAIDs) and COX‑2 inhibitors reduce PGH2 formation and thus decrease downstream prostanoids, yielding analgesic and anti-inflammatory benefits but potentially causing gastrointestinal, renal, and cardiovascular side effects. Aspirin’s antiplatelet effect is largely due to decreased TXA2 production from PGH2 in platelets.

In summary, PGH2 is best understood as the shared substrate for generating the diverse prostanoids that regulate inflammation, hemodynamics, and hemostasis.