首都医科大学学报 ›› 2000, Vol. 21 ›› Issue (3): 214-216.

• 论著 • 上一篇    下一篇

钙离子拮抗剂对大鼠局灶性脑缺血环氧酶-2的影响

龙洁, 张在强, 路敦跃   

  1. 首都医科大学附属北京天坛医院神经内科
  • 收稿日期:1999-10-22 修回日期:1900-01-01 出版日期:2000-07-15 发布日期:2000-07-15

Effect of Calcium Channel Blocker on the Expression of Cyclooxygenase-2 in Rats Focal Cerebral Ischemia

Long Jie, Zhang Zaiqiang, Lu Dunyue   

  1. Department of Neurology, Tiantan Hospital, Affiliate of Capital University of Medical Sciences
  • Received:1999-10-22 Revised:1900-01-01 Online:2000-07-15 Published:2000-07-15

摘要: 为观察钙离子拮抗剂对环氧酶-2(COX-2)表达的影响及探讨COX-2在缺血损伤过程中的作用,应用免疫组化方法,观察脑缺血模型大鼠缺血和尼莫通干预时环氧酶-2蛋白的表达。结果:2组的假手术亚组、缺血1 h和4 h亚组均无阳性染色细胞,缺血12 h后,开始出现阳性染色细胞。尼莫通组的阳性着色细胞数显著高于单纯缺血组,分别为:缺血12 h 56±11/mm2与45±18/mm2(P<0.05);缺血24 h 117±16/mm2与69±14/mm2(P<0.01);缺血48 h 81±14/mm2与41±13/mm2(P<0.01)。阳性染色仅见于梗死周围区形态完整的神经元。尼莫通组的脑梗死面积[(28.308±3.959)mm2[显著小于对照组[(46.780±6.167)mm2,P<0.01]。提示:钙离子拮抗剂可有效减轻缺血性脑损伤,在梗死周围区COX-2延迟表达以及钙离子拮抗剂增加其表达,提示COX-2存在抗缺血损伤的作用。

关键词: 脑缺血, 环氧酶-2, 钙离子拮抗剂

Abstract: To explore the potential impact of COX 2 on cerebral ischemic injurious mechanism,the present studies examined the influence of calcium channel blocker on the expression of COX 2,which is the key enzyme in arachidonic acid metabolism. The model of middle cerebral artery occlusion (MCAO) and immunohistochemistry staining were used to compare the expression of COX 2 protein in cerebral ischemic group with that in nimotop treatment group. There were no immunochemistry positive staining cells found among either the sham operation subgroup or the subgroup after MCAO for 1 and 4 h; however, positive staining cell began to acumulate after MCAO for 12 h. The positive cells in nimotop group were significantly higher than that in group without intervention: 12 h subgroup 56±11/mm 2 vs 45±18/mm 2(P< 0.05); 24 h subgroup 117±16/mm 2 vs 69±14/mm 2(P<0.01); 48 h subgroup 81±14/mm 2 vs 41±13/mm 2(P<0.01). The positive staining only occurred in intact neurons surrounding the core of the infarction. The infarcted area in nimotop group were significantly less than that in group of MCAO for 24 h[(28.308±3.959)mm 2 vs (46.780±6.167)mm 2, P<0,01). It indicated that Calcium channel blocker can effectively ameliorate experimental cerebral ischemic injury. The characteristics of delayed expression of COX 2 surrounding the core of infarct and the up regulation of COX 2 by calcium channel blocker, suggested that COX 2 may play a active role in the protective mechanism after ischemic cerebral injury.

Key words: cerebral ischemia, cyclooxygenase-2, calcium channel blocker

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