Control of cyclooxygenase-2 transcriptional activation by pro-inflammatory mediators

Prostaglandins Leukot Essent Fatty Acids. 2005 Feb;72(2):89-93. doi: 10.1016/j.plefa.2004.11.001.


Cyclooxygenase-2 (COX-2) plays a key role in diverse inflammatory conditions. Its cellular levels depend on transcriptional activation by pro-inflammatory mediators. The mechanism by which phorbol esters and cytokines activate COX-2 gene expression has been extensively characterized. Several endogenous molecules and natural products have been reported to inhibit COX-2 expression by targeting at the transcriptional activation induced by pro-inflammatory mediators. This review highlights the importance of C/EBP beta and NF-kappa B in COX-2 transcriptional activation by proinflammatory mediators and as targets of inhibition by endogenous molecules such as melatonin and natural products including salicylate and polyphenols.

Publication types

  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Animals
  • CCAAT-Enhancer-Binding Proteins / physiology
  • Cyclooxygenase 2
  • Humans
  • Inflammation Mediators / pharmacology*
  • Melatonin / pharmacology
  • Membrane Proteins
  • NF-kappa B / physiology
  • Prostaglandin-Endoperoxide Synthases / genetics*
  • Transcriptional Activation / drug effects*


  • CCAAT-Enhancer-Binding Proteins
  • Inflammation Mediators
  • Membrane Proteins
  • NF-kappa B
  • Cyclooxygenase 2
  • PTGS2 protein, human
  • Prostaglandin-Endoperoxide Synthases
  • Melatonin