中文摘要：

目的观察针刺对缺血再灌注大鼠海马区缝隙连接蛋白Cx43蛋白表达的影响。方法将Wistar大鼠随机分为正常组、模型组、非穴位针刺组及针刺组。采用改良的线栓法制备大鼠大脑中动脉局灶性脑缺血再灌注模型,模型组、非穴位针刺组及针刺组内分设4个亚组,即缺血再灌注30 min组、缺血再灌注60 min组、缺血再灌注180 min组、缺血再灌注360 min组,每组10只。针刺组电针大鼠顶中线和顶旁线;非穴位针刺组取患侧肋下髂嵴上10 mm的固定点作为针刺点;模型组不予任何处理。采用免疫组化法测Cx43蛋白表达情况。结果针刺组不同时间脑缺血再灌注后行为障碍（Bederson’s）评分与非穴位针刺组和模型组比较,差异均具有统计学意义（P〈0.05）。模型组、针刺组和非穴位针刺组不同时间脑缺血再灌注后海马Cx43灰度值与正常组比较,差异均具有统计学意义（P〈0.05）。针刺组不同时间脑缺血再灌注后海马Cx43灰度值与模型组和非穴位针刺组比较,差异均具有统计学意义（P〈0.05）。结论针刺可以阻断Cx43的过度表达,干预大脑神经元缺血再灌注损伤,在缺血性脑损伤中发挥神经保护作用。

英文摘要：

Objective To investigate the effect of acupuncture on gap junction protein Cx43 expression in the hippocampal region in ischemia/reperfusion rats. Methods Wistar rats were randomized into normal, model, non-point acupuncture and acupuncture groups. A rat model of focal cerebral ischemia/reperfusion was made by modified middle cerebral artery thread occlusion. The model, non-point acupuncture and acupuncture groups were separately divide into four subgroups： 30, 60, 180 and 360 min ischemia/reperfusion, 10 rats each. The middle and lateral lines of vertex were given electroacupuncture in the acupuncture group of rats. A subcostal fixed point 10 mm above the iliac crest on the affect side was selected as an acupuncture point in the non-point acupuncture group. The model group was not treated. Cx43 protein expression was determined by an immunohistochemical method. Results There was a statistically significant difference in the behavior disorder（Bederson＇s） score between the acupuncture group and the non-point acupuncture or model group after different times of cerebral ischemia/ reperfusion（P〈0.05）. There was a statistically significant difference in hippocampal Cx43 content between model, acupuncture or non-point acupuncture group and the normal group and between the acupuncture group and the model or non-point acupuncture group after different times of cerebral ischemia/reperfusion（P〈0.05）. Conclusions Acupuncture can inhibit the overexpression of Cx43, intervene in cerebral ischemia-reperfusion injury and produce a neuroprotective effect in ischemic brain injury.