Brune K, Beck W S, Geisslinger G, Menzel-Soglowek S, Peskar B M, Peskar B A
Department of Pharmacology and Toxicology, University of Erlangen-Nürnberg, Federal Republic of Germany.
Experientia. 1991 Mar 15;47(3):257-61. doi: 10.1007/BF01958153.
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.
使用氟比洛芬（一种手性抗炎和镇痛的2-芳基丙酸衍生物，其对映体在大鼠或人体内不会相互转化（转化率低于5%）），我们获得的证据表明，前列腺素合成抑制主要介导抗炎活性，但前列腺素合成非依赖机制有助于镇痛作用。因此，S型对映体可抑制大鼠体内前列腺素的合成、炎症反应和痛觉。R型对映体对前列腺素合成的影响小得多，且不影响炎症反应。然而，它对大鼠痛觉的阻断作用几乎与S型对映体一样有效。与R型对映体相比，S-氟比洛芬在胃肠道黏膜中明显具有致溃疡作用。这些结果表明了镇痛的其他分子机制，并提示可将R-芳基丙酸用作镇痛药。
