【摘要】 目的探讨采用慢病毒介导Bcl-2在急性脑梗死大鼠脑组织过表达对神经功能的影响。方法 45只大鼠随机分为假手术组、模型组和治疗组。假手术组和模型组分别于手术前10 d通过颅内动脉给予慢病毒空载体,治疗组给予慢病毒Bcl-2过表达载体。在采用线栓法制作大鼠大脑中动脉脑梗死模型72 h后,分析大鼠脑组织梗死范围、脑细胞凋亡指数以及神经功能的变化。结果慢病毒介导的Bcl-2表达质粒可在大鼠脑组织中表达,治疗组大鼠脑组织中Bcl-2的水平明显高于假手术组和模型组;与假手术组比较,模型组和治疗组脑组织神经细胞凋亡指数和脑组织梗死范围明显增加(P<0.05),而治疗组神经细胞凋亡指数和脑组织梗死范围较模型组明显下降(P<0.05);治疗组大鼠神经功能损伤评分较模型组明显下降(P<0.05)。结论过表达Bcl-2可降低大鼠脑组织神经细胞凋亡水平,对神经具有一定保护作用,为临床急性脑梗死治疗提供了一定的参考依据。更多还原

【Abstract】 Objective To investigate the neuroprotective effects of Bcl-2 overexpression in rats with acute cerebral infarction. Methods 45 rats were randomly divided into sham group( only isolated vascular suture unplugged,n = 15),model group( n = 15) and treatment group( n = 15). Rats in sham group and model group were treated with empty vector mediated by lentiviral. Rats in treatment group were treated with Bcl-2 overexpression mediated by lentiviral. After middle cerebral artery infarction model were constructed at 72 h,infarct size and neural function defect of brain cell were analyzed.Results Bcl-2 protein mediated by lentiviral can be expressed in rat brain. Bcl-2 protein levels in treatment group significantly increased than that of the sham group and model group( P < 0. 05). Apoptosis index and infarction range of brain tissues in model group and treatment group significantly enhanced than that of sham group( P < 0. 05). Apoptosis index and infarction range of brain tissues in treatment group significantly decreased than that of model group( P < 0. 05). Compared with sham group,neural function defect scores in model group and treatment group significantly enhanced( P < 0. 05),while those scores in treatment group significantly decreased than that of model group( P < 0. 05). Conclusion Overexpression of Bcl-2 can reduce the level of apoptosis in rat brain nerve cells and have a protective effect on nerve provides a frame of reference for the clinical treatment of acute cerebral infarction.更多还原