Fujiyoshi T, Hayashi I, Ohishi S, Kuwashima M, Iida H, Dozen M, Taniguchi N, Ikeda K, Ohnishi H
Department of Pharmacology, School of Pharmaceutical Sciences, Kitasato University, Tokyo, Japan.
Agents Actions. 1989 Jun;27(3-4):332-4. doi: 10.1007/BF01972814.
Kaolin induced a clear and reproducible writhing reaction when intraperitoneally injected into mice. A simultaneous injection (i.p.) of soybean trypsin inhibitor (SBTI) significantly suppressed the kaolin-induced writhing reaction. This writhing reaction was markedly potentiated by a simultaneous injection (i.p.) of captopril. In an in vitro experiment kaolin caused kinin-release in mouse plasma, possibly through the activation of prekallikrein. This activation of plasma prekallikrein and kinin-release were inhibited in the presence of SBTI. Some non-steroidal anti-inflammatory agents inhibited the kaolin-induced writhing reaction dose-dependently. These results suggest that kaolin-induced writhing reaction may be caused by the released bradykinin through activation of the plasma kallikrein-kinin system. This model is a novel and simple tool for assessment of analgesic agents.
将高岭土腹腔注射到小鼠体内时,会引发明显且可重复的扭体反应。同时腹腔注射大豆胰蛋白酶抑制剂(SBTI)可显著抑制高岭土诱导的扭体反应。同时腹腔注射卡托普利可使这种扭体反应明显增强。在体外实验中,高岭土可能通过激活前激肽释放酶导致小鼠血浆中激肽释放。在SBTI存在的情况下,血浆前激肽释放酶的这种激活及激肽释放受到抑制。一些非甾体抗炎药可剂量依赖性地抑制高岭土诱导的扭体反应。这些结果表明,高岭土诱导的扭体反应可能是由血浆激肽释放酶 - 激肽系统激活后释放的缓激肽引起的。该模型是评估镇痛药的一种新颖且简单的工具。