Prostaglandin synthesis and effects

Prostaglandins are always involved in the inflammatory response. PGE2 and PGI2 (prostacyclin) are the most important prostaglandins for inflammation.

Mediators that are derived from phospholipids are the so-called eicosanoids, which can be divided into two groups: the prostanoids (prostaglandins and tromboxanes) and leukotrienes.

Arachidonic acid is the starting point for both groups. When arachidonic acid is converted by cyclo-oxygenase (COX-) enzymes, the pathway of prostaglandins is entered.

Depending on the localisation different enzymes are present and thus different kinds of prostaglandins are produced.

Drug targets in prostaglandin synthesis

Different drugs interfere in the metabolic pathway of prostaglandins:


  • Glucocorticosteroids inhibit (indirectly) the phospholipase 2 (PLA2) activity.
  • NSAIDs (non-steroidal anti-inflammatory drugs) inhibit the COX-enzymes. COX-2 inhibitors specifically inhibit the COX-2.
  • Tromboxane antagonists reduce the effects of tromboxane (TxA2) at their receptor. See also aspirin in haemostasis


On the other hand prostagandins or their analogues fulfil a clinical need:


  • Labour can be induced with dinoprostone (a PGE2-analogue).
  • Epoprostenol, a PGI2-analogue, is used to inhibit platelet aggregation.
  • Misoprostol, also a PGE1-analogue, is applied in order to prevent gastrointestinal ulcers.