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目的 研究脑缺血再灌注大鼠神经细胞凋亡和原癌基因c fos、c jun表达。 方法 8周龄健康雄性Wistar大鼠 2 4只 ,随机分为缺血再灌注组、假手术组和对照组 ,每组各 8只。制作大鼠大脑中动脉栓塞 (MCAO)再灌注模型 ,缺血 4h再灌注 2h后断头处死 ,TUNEL法检测神经细胞凋亡 ,免疫组织化学法检测神经细胞c fos、c jun蛋白的表达。结果 缺血再灌注组细胞凋亡率、平均吸光度及c fos、c jun阳性细胞率、平均吸光度均高于假手术组和对照组 (P <0 .0 5 )。结论 脑缺血再灌注损伤可诱导c fos、c jun蛋白的表达和细胞凋亡 ;脑缺血再灌注大鼠神经功能评分与c fos、c jun蛋白的表达和细胞凋亡呈正相关。
Objective To investigate the neuronal apoptosis and expression of proto-oncogene c fos, c jun in cerebral ischemia-reperfusion rats. Methods Twenty-four healthy male Wistar rats of 8 weeks old were randomly divided into 4 groups: ischemia reperfusion group, sham operation group and control group, with 8 rats in each group. The model of middle cerebral artery occlusion (MCAO) reperfusion was established. The rats were sacrificed 4 hours after ischemia and reperfusion for 2 hours. The apoptosis of neurons was detected by TUNEL method. The expression of c fos and c jun proteins were detected by immunohistochemistry. Results The apoptosis rate, average absorbance, c fos, c jun positive cells rate and average absorbance in ischemia-reperfusion group were all higher than those in sham operation group and control group (P <0.05). Conclusions Cerebral ischemia / reperfusion injury can induce the expression of c fos and c jun proteins and apoptosis. The neurological function scores of cerebral ischemia / reperfusion rats were positively correlated with the expression of c fos, c jun and apoptosis.