Jugé M, Grimaud N, Petit J Y
Department of Pharmacology and Pharmacokinetics, Faculty of Pharmacy, University of Nantes, 1 rue G. Veil, Nantes Cedex, 44035, France.
Pharmacol Res. 1997 Sep;36(3):179-85. doi: 10.1006/phrs.1997.0207.
Several non-steroidal anti-inflammatory drugs of the N-pyridinyl-benzamide series that produce experimental peripheral and central anti-inflammatory effects possess a dopaminomimetic component and inhibit eicosanoid synthesis without acting directly on the enzymes classically involved in this process. We compared the anti-inflammatory and analgesic activities of one of the most active benzamide derivatives with those of clonidine. Rat paw and brain edemas were inhibited by these two agents, whereas different methods showed that yohimbine counteracted this effect and the analgesia it induced. The involvement of an alpha2-adrenergic and/or serotoninergic components in these activities is considered, without excluding the possibility that the mechanism of action is in part due to inhibition of prostaglandin synthesis.
几种具有实验性外周和中枢抗炎作用的N-吡啶基-苯甲酰胺系列非甾体抗炎药具有拟多巴胺成分,可抑制类花生酸合成,而不直接作用于经典参与该过程的酶。我们比较了最具活性的苯甲酰胺衍生物之一与可乐定的抗炎和镇痛活性。这两种药物均可抑制大鼠爪部和脑部水肿,而不同方法表明育亨宾可抵消这种作用及其诱导的镇痛作用。考虑到α2-肾上腺素能和/或5-羟色胺能成分参与这些活性,同时不排除作用机制部分归因于前列腺素合成抑制的可能性。