Hara K, Kong D L, Sharp F R, Weinstein P R
Department of Neurological Surgery, University of California, San Francisco, USA.
Neurosci Lett. 1998 Oct 30;256(1):53-6. doi: 10.1016/s0304-3940(98)00755-1.
Cyclooxygenase 2 (COX2) is the inducible isoform of COX but its involvement in ischemic neuronal injury is unclear. The effect of selective inhibition of COX2 was evaluated by intraperitoneal administration of NS-398, a selective COX2 inhibitor, before and after 2 h of temporary focal ischemia in rats. After 4 h of reperfusion, the infarct volume and the hemispheric concentration of prostaglandin E2 (PGE2), a major substance produced by COX2, were assessed. The infarct volume was unchanged by NS-398 administration. There was no difference in PGE2 levels between the ischemic and the contralateral hemispheres in the control group. However, PGE2 concentration significantly decreased in the ischemic hemisphere in the NS-398 group. The results are consistent with the previous observation that COX2 is induced in peri-ischemic areas and suggests that COX2 has a significant role in peri-ischemic pathophysiology.
环氧化酶2(COX2)是COX的诱导型同工酶,但其在缺血性神经元损伤中的作用尚不清楚。通过在大鼠短暂性局灶性缺血2小时前后腹腔注射选择性COX2抑制剂NS-398,评估选择性抑制COX2的效果。再灌注4小时后,评估梗死体积和COX2产生的主要物质前列腺素E2(PGE2)的半球浓度。给予NS-398后梗死体积未改变。对照组中,缺血半球和对侧半球的PGE2水平无差异。然而,NS-398组缺血半球的PGE2浓度显著降低。这些结果与之前在缺血周边区域诱导COX2的观察结果一致,并表明COX2在缺血周边病理生理学中具有重要作用。