Role of inducible cyclooxygenase (COX-2) in inflammation

Receptor. Spring 1994;4(1):17-23.


Nonsteroidal anti-inflammatory drugs (NSAIDs) are potent anti-inflammatory agents that act through the inhibition of the cyclooxygenase (COX) enzyme and the subsequent inhibition of prostaglandins at the site of inflammation. Unfortunately, inhibition of gastrointestinal or renal prostaglandins is associated with mechanism-based toxicities that limit the usefulness of these otherwise potent and efficacious drugs. Recently two forms of the COX enzyme have been identified: COX-1, which is constitutively expressed in many cells and tissues, and COX-2, which is selectively induced by proinflammatory cytokines at the site of inflammation. The discovery of a second COX enzyme led to the hypothesis that toxicity associated with the clinically useful NSAIDs is caused by the inhibition of COX-1, whereas the anti-inflammatory properties were caused by the inhibition of inducible COX-2. In support of this hypothesis, expression of the inducible COX-2 enzyme is selectively blocked by the potent anti-inflammatory drug dexamethasone. Selective inhibition of COX-2 may produce superior anti-inflammatory drugs with substantial safety over existing NSAIDs.

MeSH terms

  • Arachidonic Acid / metabolism
  • Cyclooxygenase Inhibitors / pharmacology*
  • Dexamethasone / pharmacology*
  • Enzyme Induction / drug effects
  • Humans
  • Inflammation / enzymology*
  • Interleukin-1 / pharmacology
  • Models, Biological
  • Prostaglandin-Endoperoxide Synthases / biosynthesis*
  • Prostaglandin-Endoperoxide Synthases / classification


  • Cyclooxygenase Inhibitors
  • Interleukin-1
  • Arachidonic Acid
  • Dexamethasone
  • Prostaglandin-Endoperoxide Synthases