摘要
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。
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.
出处
《针刺研究》
CAS
CSCD
2000年第1期8-13,共6页
Acupuncture Research
基金
国家自然科学基金! (No.39730 5 10 )
