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Bcl-2和Bax在缺血预处理保护海马神经元缺血再灌损伤中的作用
引用本文:刘亚君,崔鹤,谢东萍,缪冰,刘克敬,陈连璧.Bcl-2和Bax在缺血预处理保护海马神经元缺血再灌损伤中的作用[J].山东大学学报(医学版),2006,44(3):227-230.
作者姓名:刘亚君  崔鹤  谢东萍  缪冰  刘克敬  陈连璧
作者单位:1. 山东大学医学院生理学研究所,山东,济南,250012
2. 山东医学高等专科学校生理学教研室,山东,济南,250022
基金项目:教育部科学技术研究项目
摘    要:目的:探讨凋亡相关基因bcl-2和bax在缺血预处理(ischemic preconditioning,IPC)保护大鼠海马神经元缺血再灌损伤中的作用。方法:随机将动物分为IPC加缺血再灌组(IPC组)、单纯缺血再灌组(IR组)和对照组。观察海马CA1区神经元的组织形态学变化;TUNEL染色检测海马CA1区神经元凋亡;免疫组化测定海马CA1区神经元Bcl-2和Bax的表达。结果:IPC组海马CA1区神经元存活数显著多于IR组,凋亡细胞数显著低于IR组,Bcl-2呈强表达,Bax表达不明显。结论:IPC诱导Bcl-2表达上调和Bax蛋白表达下调,可抑制凋亡的发生,对海马CA1区神经元缺血再灌损伤起保护作用。

关 键 词:基因  bcl-2  基因  bax  缺血预处理  海马神经元  脑缺血再灌损伤  大鼠  Wistar
文章编号:1671-7554(2006)03-0227-04
收稿时间:2005-10-24
修稿时间:2005年10月24

The role of bcl-2 and bax in the protection of hippocampal neurons by cerebral ischemic preconditioning against ischemia/reperfusion injury
LIU Ya-jun,CUI He,XIE Dong-ping,MIAO Bing,LIU Ke-jing,CHEN Lian-bi.The role of bcl-2 and bax in the protection of hippocampal neurons by cerebral ischemic preconditioning against ischemia/reperfusion injury[J].Journal of Shandong University:Health Sciences,2006,44(3):227-230.
Authors:LIU Ya-jun  CUI He  XIE Dong-ping  MIAO Bing  LIU Ke-jing  CHEN Lian-bi
Institution:1. Institute of Physiology, School of Medicine, Shandong University, Jinan 250012, Shandong, China; 2. Department of Physiology, Shandong Medical College, Jinan 250022, Shandong, China
Abstract:Objective: To investigate the role of apoptotic related genes,bcl2 and bax in the protection of hippocampal neurons by cerebral ischemic preconditioning(IPC) against ischemia/reperfusion injury in rats.Methods: Rats were randomly divided into ischemic preconditioning ischemia reperfusion group(IPC), ischemia/reperfusion group(IR),and control group.Histological changes in the neurons of the hippocampal CA1 region were observed.The apoptosis of neurons in hippocampal CA1 area was determined by TUNEL staining.The expression of Bcl2 and Bax was detected with immunohistochemistry.Results: Cerebral ischemic preconditioning may increase the number of alive neurons in hippocampal CA1 region(P<0.05),markedly reduce the apoptosis of pyramidal neurons(P<0.05),and induce the expression of Bcl-2 and inhibit the expression of Bax(P<0.05).Conclusion: Cerebral ischemic preconditioning(IPC) inducing upregulation of Bcl-2 expression and downregulation of Bax expression may inhibit the apoptosis and protect the hippocampal neurons against ischemia/reperfusion injury.
Keywords:Genes  bcl-2  Genes  bax  Ischemic preconditioning  Hippocampal neurons  Cerebral ischemia/reperfusion injury  Rats  Wistar  
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