Journal of Jilin University Medicine Edition

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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

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

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