目的 :观察电针对神经细胞死亡、DNA损伤及凋亡相关基因蛋白 (Bcl 2、Bax、P53 )表达的影响。方法 :采用短暂脑缺血再灌注 (MCAo)模型

应用HE、TUNEL、免疫组织化学等实验技术进行观察。结果 :大脑中动脉阻塞 2hr后

随着再灌时间的增加梗塞灶面积进行性发展

在不同再灌时间点

电针均能减小梗塞面积

而且电针可明显减少短暂脑缺血再灌注后细胞坏死和DNA损伤

并上调Bcl 2 /Bax比值

和减少P53的表达。结论 :电针具有神经保护作用

其部分作用可能通过调节凋亡相关基因蛋白的表达而实现Objective: To observe the protective effect of electroacupuncture (EA) against rat's cerebral ischemia induced by middle cerebral artery occlusion (MCAo). Methods: 30 SD rats were randomized into ischemia (2 hr) and reperfusion (IR) control group

and IR+EA group. Each group was further divided into three subgroups respectively according to the different time course of reperfusion: IR 24 hr group

IR 48 hr group

IR 72 hr group

and EA+IR 24 hr group

EA+IR 48 hr group and EA+IR 72 hr group

with 5 rats in each group. EA was applied to "Baihui" (GV 20) and "Renzhong" (GV 26) for 1 hr beginning from 15 min on after ischemia. After 24 hours' reperfusion

EA was performed on the same two points for 45 min everyday. Neuronal death and apoptosis associated proteins (Bcl 2

Bax

P53) expressions of the cerebral tissue sections were observed using HE staining

TUNEL (TdT mediated dUTP Nick End Labeling) and immunohistochemistry. Results: After IR

the cerebral infarction area increased progressively along with the increase of duration of the reperfusion

while that of 3 EA groups was smaller. There were significant differences between IR 24 hr group and EA+IR 24 hr group

between IR 48 hr group and EA+IR 48 hr group

and between IR 72 hr group and EA+IR 72 hr group ( P <0.05～0.01).The surviving rates of neurons in the striate body of the brain of EA+IR 24 hr group and in the cerebral cortex of EA+IR 48 hr group and EA+IR 72 hr group were significantly higher than those of the corresponding IR control groups respectively ( P <0.05).The TUNEL positive cell ratio of the cerebral cortex in each one of 3 EA groups was significantly lower than that of each corresponding IR control group ( P <0.05～0.001). The ratio values of Bcl 2 positive cells/Bax positive cells of 3 EA groups were all significantly higher than those of the 3 corresponding IR control groups ( P <0.05～0.001). P53 immuno reaction positive neurons of EA+IR 24 hr group and EA+IR 48 hr group were markedly fewer than those of IR 24 hr group and IR 48 hr group respectively ( P <0.05). It showed that EA could evidently reduce the neuronal death and apoptosis

up regulated Bcl 2/Bax and down regulated the expression of P53 in cerebral IR rats. Conclusion: The protective effect of EA on cerebral ischemic neurons may be related with the resultant regulation of the expression of apoptosis associated proteins (Bcl 2

Bax

P53).