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Aspirin-like drugs may block pain independently of prostaglandin synthesis inhibition
Authors:K. Brune  W. S. Beck  G. Geisslinger  S. Menzel-Soglowek  B. M. Peskar  B. A. Peskar
Affiliation:(1) Department of Pharmacology and Toxicology, University of Erlangen-Nürnberg, Universitätsstraße 22, D-8520 Erlangen, (Federal Republic of Germany);(2) Department of Pharmacology and Toxicology, University of Bochum, Universitätsstraße 150, D-4630 Bochum 1, (Federal Republic of Germany)
Abstract:Summary Using flurbiprofen, a chiral anti-inflammatory and analgesic 2-arylpropionic acid derivative, the enantiomers of which are not converted to each other (less than 5%) in rats or man, we obtained evidence that prostaglandin synthesis inhibition is primarily mediating the anti-inflammatory activity but prostaglandin synthesis independent mechanisms contribute to the analgesic effects. Thus, the S-form inhibited prostaglandin synthesis, inflammation and nociception in rats. The R-form had much less effect on prostaglandin synthesis and did not affect inflammation. It did, however, block nociception in rats almost as potently as the S-form. S-flurbiprofen, in contrast to the R-form, was clearly ulcerogenic in the gastrointestinal mucosa. These results indicate additional molecular mechanisms of analgesia and suggest the use of R-arylpropionic acids as analgesics.
Keywords:Aspirin-like drugs  flurbiprofen enantiomers  anti-inflammatory  analgesic  gastrointestinal toxicity  prostaglandin synthesis  rat
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