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异丙酚对大鼠脑缺血再灌注后脑细胞凋亡和Bcl-2、Caspase-3蛋白表达的影响
引用本文:杨宾侠,陈卫,张煜东,赵砚丽.异丙酚对大鼠脑缺血再灌注后脑细胞凋亡和Bcl-2、Caspase-3蛋白表达的影响[J].国际麻醉学与复苏杂志,2006,27(2):85-87,124.
作者姓名:杨宾侠  陈卫  张煜东  赵砚丽
作者单位:河北省人民医院麻醉科,石家庄市,050071
摘    要:脑缺血再灌注后脑损伤的发病机制较复杂,其所致病理损伤包括细胞坏死和凋亡。细胞凋亡与脑缺血再灌注损伤关系密切,是神经元迟发性死亡的主要形式。研究提示与凋亡密切相关的Bcl-2、Caspase-3蛋白等参与了这种迟发性死亡,它们表达的量决定了细胞的生存。本实验采用流式细胞仪、

关 键 词:Caspase-3蛋白  脑缺血再灌注损伤  脑细胞凋亡  Bcl-2  蛋白表达  异丙酚  大鼠  免疫组化法检测  迟发性死亡  流式细胞仪

The effect of propofol on cell apoptosis and expression of Bcl-2 and caspase-3 protein of focal cerebral ischemia -reperfusion in the rats
YANG Bin-xia ,CHEN Wei, ZHANG Yu-dong , et al.The effect of propofol on cell apoptosis and expression of Bcl-2 and caspase-3 protein of focal cerebral ischemia -reperfusion in the rats[J].international journal of anesthesiology and resuscitation,2006,27(2):85-87,124.
Authors:YANG Bin-xia  CHEN Wei  ZHANG Yu-dong  
Affiliation:Department of Anesthesiology,He bei provice people hospital, Shijiazhuang 050071 ,china
Abstract:Objective To investgate the effects of propofol on cell apoptosis of focal cerebral ischemia-reperfusion injury in the rat model of reversible middle cerebral artery occlusion(MCAO).Methods Male SD rats were used to undergo 2 h MCAO and 2 h reperfusion 2.Brain cell apopotosis and expression of bcl-2 protein was measured by flow cytometry(FCM),expression of caspase-3 protein was observed by immunohistochemical method;brain cell structure was examined under light microscope.Results Propofol could significantly inhibit the apoptosis of brain cell after focal cerebral ischemia-reperfusion.Compared to sham group,caspase-3 protein positive-staining cells were remarkably increased in control group,while propofol group were remarkably decreased.Pretreatment of animals with propofol before reperfusion significantly increased the Fluorescent index of Blc-2.Conclusion The increased expression of Caspase-3 may be an important mechanism for brain cell apoptosis after brain ischemia-reperfusion.Propofol possesses the antiapoptotic effects which may be related to the reduction of the expreesion of caspase-3 and increasing the expression of Bcl-2 protein.
Keywords:propofol  cerebral ischemia  reperfusion injury  brain cell apoptosis  
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