作者: F. A. KUEHL , J. L. HUMES , R. W. EGAN , E. A. HAM , G. C. BEVERIDGE
DOI: 10.1038/265170A0
关键词:
摘要: SINCE the discovery that non-steroidal anti-inflammatory agents (NSAI) are potent inhibitors of prostaglandin synthetase1–3, there has been controversy about role primary prostaglandins (PGEs+PGFs=PGs) in inflammatory diseases. A parallel demonstrated between ability drugs such as indomethacin and aspirin to inhibit cyclo-oxygenase, initial step leading formation PGs, activity4–6. The failure administered PGs fully mimic inflammation processes, however, is not consistent with this concept7,8, further studies have shown other products derived from reaction cyclo-oxygenase arachidonic acid (PGG2, PGH2 thromboxane A2) although quite labile, biological activities exceeding potency themselves9,10. Since these ephemeral mediators also subject regulation by NSAI they too must be considered potential causal inflammation. We investigated possibility examining action several on total pattern oxygenation products. results indicate endoperoxide PGG2 a pivotal acute