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Pharmazentrum Frankfurt, Klinikum der Johann Wolfgang Goethe-Universität, Frankfurt, 60590 Frankfurt am Main, Germany
1Correspondence: Pharmazentrum Frankfurt, Klinikum der Johann Wolfgang Goethe-Universität, Theodor Stern Kai 7, 60590 Frankfurt am Main, Germany. E-mail: geisslinger{at}em.uni-frankfurt.de
Several studies have demonstrated unequivocally that certain
nonsteroidal anti-inflammatory drugs (NSAIDs) such as sodium
salicylate, sulindac, ibuprofen, and flurbiprofen cause
anti-inflammatory and antiproliferative effects independent of
cyclooxygenase activity and prostaglandin synthesis inhibition. These
effects are mediated through inhibition of certain transcription
factors such as NF-
B and AP-1. The respective NSAIDs might interfere
directly with the transcription factors, but their effects are probably
mediated predominantly through alterations of the activity of cellular
kinases such as IKKß, Erk, p38 MAPK, or Cdks. These effects
apparently are not shared by all NSAIDs, since indomethacin failed to
inhibit NF-B and AP-1 activation as well as Erk and Cdk activity. In
contrast, indomethacin was able to activate PPAR
, which was not
affected by sodium salicylate or aspirin. The differences in
cyclooxygenase-independent mechanisms may have consequences for the
specific use of these drugs in individual patients because additional
effects may either enhance the efficacy or reduce the toxicity of the
respective compounds.—Tegeder, I., Pfeilschifter, J., Geisslinger, G.
Cyclooxygenase-independent actions of cyclooxygenase inhibitors
Key Words: aspirin • NSAIDs • apoptosis • metalloproteinase
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