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(ĐTĐ) – A prostaglandin is any member of a group of lipid compounds that are derived enzymatically from fatty acids and have important functions in the animal body. Every prostaglandin contains 20 carbon atoms, including a 5-carbon ring.

They are mediators and have a variety of strong physiological effects, such as regulating the contraction and relaxation of smooth muscle tissue. Prostaglandins are not hormones, but autocrines or paracrines, which are locally acting messenger molecules. They differ from hormones in that they are not produced at a discrete site but in many places throughout the human body. Also, their target cells are present in the immediate vicinity of the site of their excretion (of which there are many).

The prostaglandins, together with the thromboxanes and prostacyclins, form the prostanoid class of fatty acid derivatives, a subclass of eicosanoids.

History and name

The name prostaglandin derives from the prostate gland. When prostaglandin was first isolated from seminal fluid in 1935 by the Swedish physiologist Ulf von Euler,2 and independently by M.W. Goldblatt, it was believed to be part of the prostatic secretions. (In fact, prostaglandins are produced by the seminal vesicles). It was later shown that many other tissues secrete prostaglandins for various functions. The first total syntheses of prostaglandin F2a and prostaglandin E2 were reported by E. J. Corey in 1969.In 1971, it was determined that aspirin-like drugs could inhibit the synthesis of prostaglandins. The biochemists Sune K. Bergström, Bengt I. Samuelsson and John R. Vane jointly received the 1982 Nobel Prize in Physiology or Medicine for their research on prostaglandins.



Prostaglandins are found in most tissues and organs. They are produced by all nucleated cells except lymphocytes. They are autocrine and paracrine lipid mediators that act upon platelets, endothelium, uterine and mast cells. They are synthesized in the cell from the essential fatty acids (EFAs).

An intermediate is created from phospholipase-A2, then brought out of one of either the cyclooxygenase pathway or the lipoxygenase pathway to form either prostaglandin and thromboxane or leukotriene respectively. The cyclooxygenase pathway produces thromboxane, prostacyclin and prostaglandin D, E and F. The lipoxygenase enzyme pathway is inactive in leukocytes and in macrophages and synthesizes leukotrienes.

NameEFA TypeSeries
Gamma-linolenic acid (GLA) via DGLAω-6series-1
Arachidonic acid (AA)ω-6series-2
Eicosapentaenoic acid (EPA)ω-3series-3

Release of prostaglandins from the cell

Prostaglandins were originally believed to leave the cells via passive diffusion because of their high lipophilicity. The discovery of the prostaglandin transporter (PGT, SLCO2A1), which mediates the cellular uptake of prostaglandin, demonstrated that diffusion cannot explain the penetration of prostaglandin through the cellular membrane. The release of prostaglandin has now also been shown to be mediated by a specific transporter, namely the multidrug resistance protein 4 (MRP4, ABCC4), a member of the ATP-binding cassette transporter superfamily. Whether MRP4 is the only transporter releasing prostaglandins from the cells is still unclear.


Prostaglandins are produced following the sequential oxidation of AA, DGLA or EPA by cyclooxygenases (COX-1 and COX-2) and terminal prostaglandin synthases. The classic dogma is as follows:

  • COX-1 is responsible for the baseline levels of prostaglandins.
  • COX-2 produces prostaglandins through stimulation.

However, while COX-1 and COX-2 are both located in the blood vessels, stomach and the kidneys, prostaglandin levels are increased by COX-2 in scenarios of inflammation. A third form of COX, termed COX-3 is thought to exist in the brain and may be associated with relief of Headaches when on NSAID therapy.

Prostaglandin E synthase

Prostaglandin E2 (PGE2) is generated from the action of prostaglandin E synthases on prostaglandin H2 (PGH2). Several prostaglandin E synthases have been identified. To date, microsomal prostaglandin E synthase-1 emerges as a key enzyme in the formation of PGE2.


Biosynthesis of eicosanoids. (series-2)

Other terminal prostaglandin synthases

Terminal prostaglandin synthases have been identified that are responsible for the formation of other prostaglandins. For example, hematopoietic and lipocalin prostaglandin D synthases (hPGDS and lPGDS) are responsible for the formation of PGD2 from PGH2. Similarly, prostacyclin (PGI2) synthase (PGIS) converts PGH2 into PGI2. A thromboxane synthase (TxAS) has also been identified. Prostaglandin F synthase (PGFS) catalyzes the formation of 9α,11β-PGF2α,β from PGD2 and PGF from PGH2 in the presence of NADPH. This enzyme has recently been crystallyzed in complex with PGD2 and bimatoprost (a synthetic analogue of PGF).


There are currently ten known prostaglandin receptors on various cell types. Prostaglandins ligate a sub-family of cell surface seven-transmembrane receptors, G-protein-coupled receptors. These receptors are termed DP1-2, EP1-4, FP, IP1-2, and TP, corresponding to the receptor that ligates the corresponding prostaglandin (e.g., DP1-2 receptors bind to PGD2).

The ersity of receptors means that prostaglandins act on an array of cells and have a wide variety of effects such as:

  • cause constriction or dilation in vascular smooth muscle cells
  • cause aggregation or disaggregation of platelets
  • sensitize spinal neurons to pain
  • decrease intraocular pressure
  • regulate inflammatory mediation
  • regulate calcium movement
  • control hormone regulation
  • control cell growth
  • acts on thermoregulatory center of hypothalamus to produce fever
  • acts on mesangial cells in the glomerulus of the kidney, to increase Glomerular filtration rate

Prostaglandins are potent but have a short half-life before being inactivated and excreted. Therefore, they send only paracrine (locally active) or autocrine (acting on the same cell from which it is synthesized) signals.


The following is a comparison of different types of prostaglandin, prostaglandin I2 (PGI2), prostaglandin E2 (PGE2), and prostaglandin F2a (PGF2a).

  • vasodilation
  • inhibit platelet aggregation
  • bronchodilatation
  • bronchoconstriction
  • GI tract smooth muscle contraction
  • bronchodilatation
  • GI tract smooth muscle relaxation
  • vasodilatation
  • ↓ gastric acid secretion
  • ↑ gastric mucus secretion
  • uterus contraction (when pregnant)
  • GI tract smooth muscle contraction
  • lipolysis inhibition
  • ↑ autonomic neurotransmitters
  • ↑ platelet response to their agonists and ↑ atherothrombosis in vivo
  • hyperalgesia
  • pyrogenic
  • uterus contraction
  • bronchoconstriction

Role in pharmacology


Examples of prostaglandin antagonists are:

  • NSAIDs (inhibit cyclooxygenase)
  • Corticosteroids (inhibit phospholipase A2 production)
  • COX-2 selective inhibitors or coxibs
  • Cyclopentenone prostaglandins may play a role in inhibiting inflammation

Clinical uses

Synthetic prostaglandins are used:

  • To induce childbirth (parturition) or abortion (PGE2 or PGF2, with or without mifepristone, a progesterone antagonist);
  • To prevent closure of patent ductus arteriosus in newborns with particular cyanotic heart defects (PGE1)
  • To prevent and treat peptic ulcers (PGE)
  • As a vasodilator in severe Raynaud’s phenomenon or ischemia of a limb
  • In pulmonary hypertension
  • In treatment of glaucoma (as in bimatoprost ophthalmic solution, a synthetic prostamide analog with ocular hypotensive activity)
  • To treat erectile dysfunction or in penile rehabilitation following surgery (PGE1 as alprostadil).
  • To treat egg binding in small birds
  • As an ingredient in eyelash and eyebrow growth beauty products due to side effects associated with increased hair growth

Source: Wikipedia

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