Aspirin has diverse clinical effects mediated through the inhibition of cyclooxygenase isoforms (COX-1 and COX-2).
This fascinating but simple and cheap drug has an assured future Ask any medical student and he or she will tell you that aspirin reduces fever, pain, and inflammation but may cause ulcers. Students may also recollect that it prolongs bleeding, and may prevent strokes and heart attacks, but would be unlikely to know of its use in cancer or Alzheimer's disease. A defining point in the history of aspirin was the discovery that it inhibited the prostaglandin forming cyclooxygenase.1 Prostaglandins cause inflammation, fever, and pain; have gastric cytoprotective actions; and are implicated in platelet aggregation, so this discovery provided a unified explanation for the effects of aspirin (and most other non-steroidal anti-inflammatory drugs). However, events took an even more interesting turn when a further isoform of cyclo-oxygenase, cyclooxygenase-2, was discovered.2 While similar in many ways to the original enzyme (COX 1) there were important differences, including the fact that COX 2 was induced in cells by inflammatory insults. COX 2 therefore seemed to be the most relevant target in inflammation, which led …
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R J Flower (2003) studied this question.
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