中文摘要：

目的：探讨电针对脑缺血大鼠海马神经元凋亡的作用及可能内在机制。方法：将90只雄性SD大鼠随机分为假手术组、模型组、电针组、电针＋PKA抑制剂（H89）组和电针＋生理盐水（Ns）组，每组又分为7d、14d、21d3个亚组。制备双侧颈总动脉永久性结扎（2VO）模型；电针百会穴（GV20）和大椎穴（GV14）；通过TUNEL法和免疫蛋白印迹法观测海马神经元凋亡及Bax蛋白、Bcl-2蛋白表达量。结果：各组大鼠组内3个时间点间的海马神经元凋亡率相比，模型组14d组、21d组较7d组显著增加（P〈O．05）；其余各组各时间点差异均无统计学意义。凋亡相关蛋白表达量比较，电针组21d组较14d组Bcl-2蛋白量显著增多（P〈0．05）。其余各组各个评价指标在3个时间点比较差异无统计学意义。同时间点各组大鼠间海马神经元凋亡率比较，模型组较假手术组均显著增加（P〈0．05）；电针组较模型组均显著降低（P〈0．05）；电针＋H89组较电针＋NS组均显著增多（P〈0．05）。同时间点各组大鼠间的凋亡相关蛋白表达量比较，模型组较假手术组Bax蛋白量均显著增高（P〈0．05），而Bcl-2蛋白量均显著降低（P〈0．05）；电针组较模型组Bax蛋白量均显著降低（P〈o．05），而Bcl-2蛋白量均显著增加（P〈0．05）；电针＋H89组较电针q-NS组Bax蛋白量均明显增多（P〈0．05），而Bcl-2蛋白量明显降低（P〈0．05），但在14d时2组Bcl-2蛋白表达差异无显著统计学意义。结论：电针百会穴和大椎穴可抑制Bax蛋白表达，促进Bcl-2蛋白表达而减轻脑缺血大鼠海马神经元凋亡，给予H89后电针的作用被抑制，说明电针抗凋亡作用的内在机制可能与激活PKA-CREB信号通路相关。

英文摘要：

Objective： To investigate whether electroacupuncture （EA） protects hippocampal neurons from apopto- sis and its probable mechanism in rats following cerebral hypoperfusion. Methods： Ninety male Sprague-Dawley （819） rats were randomly divided into five groups： a sham-operated control group （Con）, a model group （Mod）, an EA group （EA）, an EA combined with intracerebroventricular （ICV） injection of PKA blocker H89 group （EA＋ H89） and an EA combined with ICV injection of normal saline （NS） group （EA＋NS）. Each group included three time courses： 7 days, 14 days and 21 days. Cerebral hypoperfusion was induced by permanent and bilateral common carotid artery occlusion （2-vessel occlusion, 2VO）. EA was given on GV20 and GV14. TUNEL and Western blot- ting were employed to observe apoptosis of neurons and expression changes of Bax and Bcl-2 proteins of the hippo- campus. Results： In the Mod group, the apoptosis rate was significantly higher on day 14 and 21 than on day 7 （P〈0.05）, and there was no significant difference in other groups among the three time points. In the EA group, the expression of Bcl-2 protein was significantly higher in the 21-day subgroup than in the 14-day subgroup （P〈0. 05）, and there were no significant differences in other groups. Percentages of apoptotic neurons were higher in the Modgroup than in the Con group （P~0. 05）, but lower in the EA group than in the Mod group （P〈0. 05）. In the EA＋H89 group, protecting effects of EA were weakened, and those in the EA＋NS group had no sig- nificant change. Western blotting suggested that the expression of Bax protein was signi{icantly up-regulated （P〈0. 05） and that of Bcl-2 protein significantly down-regulated （P〈0. 05） in the Mod group as compared with the Con groups, and the Bax protein significantly reduced （P〈0. 05） and the Bcl-2 protein significantly increased （P〈0. 05） in the EA group as compared with the Mod group. In the EAq-H89 group, the Bax pro