首页> 中文期刊> 《南昌大学学报(医学版)》 >脑缺血再灌注损伤模型大鼠大脑皮质细胞色素C与Bax蛋白的表达

脑缺血再灌注损伤模型大鼠大脑皮质细胞色素C与Bax蛋白的表达

         

摘要

目的 制备局灶性脑缺血再灌注损伤大鼠模型,并观察大脑皮质细胞色素C(CytC)与Bax蛋白表达的变化.方法 采用随机数字表法将22只雄性SD大鼠分为正常组(6只)、假手术组(6只)和模型组(10只).采用线栓法闭塞大脑中动脉2 h后进行再灌注3 d,制备局灶性脑缺血再灌注损伤模型.采用神经缺失评分观察大鼠的行为学表现;TTC染色检查脑组织梗死情况;HE染色观察大鼠脑组织形态结构;Western blot技术检测大鼠大脑皮质CytC与Bax蛋白的表达.结果 假手术组大鼠无神经功能障碍表现,脑组织未见梗死灶,脑组织神经细胞形态规则;大脑皮质CytC与Bax蛋白的相对表达量,与正常组相比差异无统计学意义(P>0.05).与假手术组相比,模型组大鼠出现神经功能障碍,左侧半球可见梗死灶,梗死侧脑组织形态学观察可见神经细胞大量坏死脱落,胞质呈空泡变性、疏松,胞核浓缩深染;大脑皮质CytC与Bax蛋白表达量明显增加(P<0.05).结论 大脑中动脉闭塞2 h 后进行再灌注3 d可造成脑缺血再灌注损伤,可能与大脑皮质CytC与Bax蛋白的表达增加有关.%Objective To establish a rat model of focal ischaemia-reperfusion injury , and to observe the changes in cytochrome C and Bax protein expression in cerebral cortex . Methods Twenty-two male SD rats were randomly divided into three groups :normal group (n= 6 ), sham-operated group group (re-6) and model group (n-10) .Focal cerebral ischemia-reperfusion injury was induced by middle cerebral artery occlusion for 2 hours and reperfusion for 3 days .Behavioral performance,brain infarction ,brain morphology and cortical expression of cytochrome C and Bax protein were measured using Neurologic Deficit Score ,TTC staining , HE staining and Western blotting respectively .Results Rats in sham-operated group showed regular neuronal cell morphology without neurological dysfunction and brain infarction . There were no significant differences in cortical expression of cytochrome C and Bax protein between sham -operated group and normal group (P>0 .05 ) .Compared with sham-operated group ,cortical expression of cytochrome C and Bax protein significantly increased in model group (p<0 .05 ) .In addition ,rats in model group showed neurological dysfunction ,left hemisphere infarction , neuronal cell necrosis , cyto-plasmic vacuolar degeneration ,and deeply stained nucleus .Conclusion Middle cerebral artery occlusion (MCAO) for 2 hours and reperfusion for 3 days can induce cerebral ischemia-reperfusion injury ,which may be correlated with the increase in the expression of cytochrome C and Bax pro -tein.

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