吉林大学学报(医学版)

• 基础研究 • 上一篇    下一篇

尼莫地平对局灶性脑缺血再灌注损伤大鼠脑神经元的
保护作用及其机制

韩 威1,2,姜慧轶3,魏胜男4,孟昭杰4,戴丽君2   

  1. 1.江苏大学化工学院,江苏 镇江212013;2.吉林省脑科医院神经内科,吉林 四平136000;3. 吉林大学第一医院儿科,吉林 长春 130021;4.吉林大学基础医学院药理学系,吉林 长春130021
  • 收稿日期:2013-08-29 出版日期:2014-05-28 发布日期:2014-06-05
  • 通讯作者: 韩 威(Tel:0434-5089387,E-mail:davy1976@126.com) E-mail:davy1976@126.com
  • 作者简介:韩 威(1976-),女,吉林省四平市人,副主任医师,医学博士,在站医学博士 后,主要从事脑血管临床与基础的研究。
  • 基金资助:

    吉林省卫生厅科研基金资助课题(2010ZC032)

Protective effect  of  nimodipine  on neuron of rats with focal
 cerebral ischemia-reperfusion injury and its mechanism

HAN Wei1,2,JIANG Hui-yi3,WEI Sheng-nan4,MENG Zhao-jie4,DAI Li-jun2    

  1. 1.School of Chemical Industry,Jiangsu University,Zhenjiang 212013,China;2. Department of Neurology,Brain Hospital of Jilin Province,Siping 136000,China;3.Department of Pediatrics,First Hospital,Jilin University, Changchun 130021,China;4. Department of Pharmacology,School of Basic Medical Sciences,Jilin University,Changchun 130021,China
  • Received:2013-08-29 Online:2014-05-28 Published:2014-06-05

摘要:

目的: 探讨尼莫地平对局灶性脑缺血再灌注损伤大鼠脑神经元的保护作用及其对Bax和Bcl-2蛋白表达的影响并阐明其作用机制。方法:30只雄性Wistar大鼠随机分
为假手术组、模型组和尼莫地平组,每组10只。采用线栓法堵塞大鼠大脑中动脉制作脑缺血再灌注损伤模型。缺血2 h再灌注2 h后进行神经功能学评分。之后断头取脑,应用TUNEL染色及SP免疫组织化学方法观察脑组织梗死情况并检测Bax和Bcl-2蛋白的表达水平。结果:与模型组比较,尼莫地平组大鼠脑组织凋亡细胞数明显减少(P<0.05),Bax蛋白表达水平减少(P<0.05),Bcl-2蛋白表达水平增加(P<0.05)。形态学观察,模型组大鼠脑细胞坏死严重,水肿明显;尼莫地平组大鼠脑组织坏死细胞数减少,水肿情况有所改善。结论:尼莫地平对局灶性脑缺血再灌注损伤大鼠脑组织具有保护作用,其作用可能是通过下调Bax和上调Bcl-2相关蛋白表达从而抑制
脑神经元凋亡实现的。

关键词:  , 尼莫地平, 脑缺血再灌注损伤, 细胞凋亡, Bax蛋白, Bcl-2蛋白

Abstract:

Objective To investigate the protective effect of nimodipine on neuron of the rats with focal cerebral ischemia-reperfusion injury and the expressions of Bax and Bcl-2,and to clarify their mechanisms. Methods The focal cerebral-ischemia reperfusion model was induced by the middle cerebral artery occlusion(MCAO)
 method. 30 male Wistar rats were randomly divided into sham operation,model,and nimodipine  groups(n=10). The neurological deficit score was performed after 2 h ischemia following 2 h reperfusion. The infarction was observed by TUNEL staining and the expressions of Bax and Bcl-2 were detected by SP immunohistochemistry method. Results Compared with model group,the number of apoptotic cells of the rats in nimodipine group was significantly decreased(P<0.05),the expression of Bax  was significantly decreased (P<0.05),and the  Bcl-2 expression was increased significantly(P<0.05).The morphological examination showed that the neurons of the rats in model group had  serious necrosis and edema while  the number of  dead cells in nimodipine treatment group  was reduced and the edema was improved.Conclusion Nimodipine has a protective effect on brain tissue of the rats with focal cerebral ischemia-reperfusion injury,which is
closely related to the down-regulation  of Bax and up-regulation of Bcl-2 and inhibition of the apoptosis of neuron.

Key words: nimodipine, cerebral ischemia-reperfusion injury, apoptosis, Bax protein, Bcl-2 protein

中图分类号: 

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