Effect of selective inhibition of cyclooxygenase 2 on temporary focal cerebral ischemia in rats
Effect of selective inhibition of cyclooxygenase 2 on temporary focal cerebral ischemia in rats
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DOI：
10.1016/s0304-3940(98)00755-1
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发表时间：
1998-10-30
影响因子：
2.5
通讯作者：
Weinstein, PR
中科院分区：
文献类型：
--
作者：
Hara, K;Kong, DL;Weinstein, PR
环氧合酶2(COX2)是环氧合酶的诱导型亚型，但其在缺血性神经元损伤中的作用尚不清楚。在大鼠局灶性短暂性脑缺血2 h前后，通过腹腔注射选择性COX2抑制剂NS-398来评价选择性抑制COX2的作用。再灌流4h后，测定脑梗塞体积和脑内COX2产生的主要物质前列腺素E2(PGE2)浓度。给予NS-398后，脑梗塞体积无明显变化。对照组缺血侧和对侧大脑半球PGE2水平差异无统计学意义。而NS-398组缺血侧PGE2浓度显著降低。这一结果与先前关于COX2在缺血区诱导表达的观察结果一致，提示COX2在缺血区的病理生理机制中具有重要作用。(C)1998由爱思唯尔科学爱尔兰有限公司出版。保留所有权利。
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. (C) 1998 Published by Elsevier Science Ireland Ltd. All rights reserved.