The anti-inflammatory activity of aspirin: the active metabolite

  • M. J. H. Smith
Part of the Inflammation: Mechanisms and Treatment book series (FTIN, volume 4)


It was suggested by Vane1 in 1971 that the major therapeutic effects of aspirin and of other non-steroidal acidic drugs were explicable in terms of an interference with the biosynthesis of prostaglandins. The basis of the idea was the finding that aspirin could inhibit the activity of the so-called prostaglandin synthetase enzyme system under in vitro conditions. The hypothesis has been restated in later years in a more explicit fashion. Thus, Gryglewski2 concluded that the target biomolecule for NSAID is fatty acid cyclo-oxygenase and that inhibition of prostaglandin generation in vivo accounts for the therapeutic effectiveness of acidic NSAID. The evidence supporting this mechanism of action has been largely concerned with the analgesic and antipyretic effects of aspirin. It is, however, less acceptable as an exclusive mode of action for the anti-inflammatory and anti-rheumatic actions of aspirin and similar drugs3–5. Nevertheless, some authors such as Katler and Weissman6 adhere to the view that the anti-inflammatory effects of aspirin and indomethacin can be explained almost entirely by virtue of their ability to inhibit cyclo-oxygenase, thus preventing the transformation of arachidonic acid to both prostaglandins and thromboxanes. The aims of the present communication are, first, to review the evidence that aspirin and salicylic acid inhibit the enzyme activity in vitro. Secondly, to examine the mechanisms by which aspirin interferes with prostaglandin biosynthesis in vivo.


Salicylic Acid Inflammatory Exudate Prostaglandin Biosynthesis Gentisic Acid Prostaglandin Synthetase 
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Copyright information

© MTP Press Limited 1980

Authors and Affiliations

  • M. J. H. Smith
    • 1
  1. 1.UK

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