杨秋生, 原田芳照, 鹿取信. 角叉菜诱导大鼠胸膜炎中环氧酶-2的生成及NS-398对其选择性抑制作用J. 药学学报, 1999, 34(3): 181-184.
引用本文: 杨秋生, 原田芳照, 鹿取信. 角叉菜诱导大鼠胸膜炎中环氧酶-2的生成及NS-398对其选择性抑制作用J. 药学学报, 1999, 34(3): 181-184.
Yang Qiusheng, Harada Yoshiteru, Katori Makoto. INDUCTION OF CYCLOOXYGENASE-2 IN RAT CARRAGEENIN-INDUCED PLEURISY AND ITS SELECTIVE INHIBITION BY NS-398J. Acta Pharmaceutica Sinica, 1999, 34(3): 181-184.
Citation: Yang Qiusheng, Harada Yoshiteru, Katori Makoto. INDUCTION OF CYCLOOXYGENASE-2 IN RAT CARRAGEENIN-INDUCED PLEURISY AND ITS SELECTIVE INHIBITION BY NS-398J. Acta Pharmaceutica Sinica, 1999, 34(3): 181-184.

角叉菜诱导大鼠胸膜炎中环氧酶-2的生成及NS-398对其选择性抑制作用

INDUCTION OF CYCLOOXYGENASE-2 IN RAT CARRAGEENIN-INDUCED PLEURISY AND ITS SELECTIVE INHIBITION BY NS-398

  • 摘要: 目的:检测角叉菜诱导的大鼠胸膜炎渗出细胞中COX-2的存在并观察NS-398对其活性的影响。方法:用SDS-PAGE和Western blot分析及PGHS-1和PGHS-2抗血清,识别并检测胸膜炎渗出细胞中的COX-2。酶活性用TLC法测定。结果:致炎后5 h, PGHS-2出现, 19 h时消失,而PGHS-1在注射角叉菜前后均出现。此外,在胸膜炎大鼠和正常大鼠的肺、胃、肾微粒体中,只检测到PGHS-1, 未检测到PGHS-2。新的非甾体抗炎药NS-398,可明显抑制COX-2活性(IC50=4.5 μmol.L-1 )。 结论:COX-2仅存在于角叉菜诱导的炎症部位;NS-398可选择性抑制COX-2,并呈剂量依赖性。

     

    Abstract: AIM: To detect cyclooxygenase-2(COX-2)/prostaglandin H synthase-2(PGHS-2) in cells of pleural exudate and investigate the effect of NS-398 on its activity. METHODS: COX-2 was tested by SDS-PAGE and Western blot in cells of the pleural exudate induced in rats by intrapleural injection of 0.2 ml of 2% carrageenin. TLC was used to analyze the activity of COX-2. RESULTS: The examination using PGHS-1 or PGHS-2 antiserum showed that PGHS-2 appeared at the 5th hour after carrageenin injection, and vanished at the 19th hour. While, PGHS-1 appeared in cells before and after carrageenin injection. Furthermore, only PGHS-1, but not PGHS-2, was detected in the microsomal fraction of the lung, stomach and kidney of pleurisy-affected and normal control rats. NS-398, a novel nonsteroidal anti-inflammatory agent, suppressed the activity of COX-2 with IC50=4.5 μmol.L-1. CONCLUSION: COX-2 is only present in inflammatory site induced by carrageenin. NS-398 may selectively inhibit COX-2 activity in a dose-dependent manner.

     

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