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Cyclo-oxygenase 1 and cyclo-oxygenase 2

Last reviewed dd mmm yyyy. Last edited dd mmm yyyy

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  • non-steroidal anti-inflammatory drug (NSAID)s are thought to work via inhibition of the enzyme, cyclo-oxygenase (COX), also known as prostaglandin synthetase
    • NSAIDs are a heterogeneous class including aspirin and various other nonselective and selective inhibitors of cyclooxygenase (COX). Aspirin is the only NSAID used for prevention and treatment of coronary heart disease (CHD)

  • cyclo-oxygenase is present in different forms - the two isoforms are encoded by different genes and have unique patterns of expression:
    • cyclo-oxygenase 1 (COX1)
      • COX-1 isozyme is essential for the maintenance of normal physiologic states in many tissues including the kidney, gastrointestinal tract, and platelets - for example, COX-1 activation in the gastric mucosa leads to prostaglandin PGI2 (prostacyclin) production, which is cytoprotective
      • thromboxane A2, which is primarily synthesized in platelets through COX-1 activity, causes platelet aggregation, vasoconstriction, and smooth muscle proliferation
    • cyclo-oxygenase 2 (COX2) is less widely expressed, but is readily induced by pro-inflammatory stimuli, and catalyses production of prostaglandins that mediate inflammation
    • inhibition of COX-1 is thought to be the main way in which NSAIDs cause gastrointestinal damage
      • anti-inflammatory efficacy is believed to result from inhibition of COX-2
      • at therapeutic doses, COX-2 inhibitors inhibit COX-2 but not COX-1, so it was postulated that they should relieve inflammation with less gastrointestinal toxicity than conventional NSAIDs
      • it now is apparent that selective inhibition of COX-2 appears more complex than first suggested, as COX-2 has many other functions besides its role in inflammation
        • in vascular endothelium, it mediates production of prostaglandin PGI2 (prostacyclin), a vasodilator and inhibitor of both platelet aggregation and proliferation of vascular smooth muscle cells
        • therefore in consideration that COX-1 mediates synthesis of thromboxane A2 (vasoconstrictor and stimulator of both platelet aggregation and vascular proliferation) both isoforms are probably important in vascular homeostasis and regulation of platelet function

Reference:

  1. Prescribers' Journal (1999); 39 (2): 102-8.
  2. Drug and Therapeutics Bulletin (2005); 43(1):1-6.

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