采用暂时性脑缺血再灌注模型和组织化学、TUNEL细胞标记等实验技术

观察神经细胞死亡和一氧化氮合酶 (NitricOxideSynthase

NOS)水平的变化。实验结果表明

暂时性脑缺血再灌注时脑内NOS表达显著增加

且引起延迟性细胞死亡

包括坏死与凋亡。电针可明显减少神经细胞坏死

在存活细胞增多的基础上

TUNEL阳性细胞的比例有所增加 ;与此同时

电针亦使脑内NOS表达显著减弱。提示电针具有神经保护作用

且可能与其下调NOS、减少NO的过量生成有关Transient cerebral ischemia/reperfusion model was adopted

and the method of TUNEL(TdT mediated dUTP Nick End Labeling)

immunohistochemistry are used to observe the neuronal death and change of nitric oxide synthase level. The results showed that transient cerebral ischemia/reperfusion evidently increased the expression of NOS

as well as induced the delayed neuronal death

which included both necrosis and apoptosis. EA evidently decreased the expression of NOS and necrotic neuron loss

increased the percent of apoptotic cells and survived cells. It sugested that EA protective effect may be related with reducing the increased NOS and decreasing the excess production of NO.