中文摘要：

目的：探讨电针是否通过干预Bax／Bcl-2mRNA的表达，来调控缺血再灌注大鼠大脑皮层细胞凋亡，发挥电针对脑神经元保护作用。方法：将清洁级健康雄性SD大鼠19只，按随机数字表随机分成假手术组（n=5）和用于造模动物14只，采用改良Longa线栓大脑中动脉法制作局灶性脑缺血再灌注模型。在成功制作出脑缺血再灌注模型并作神经缺损综合评分为2分以上后随机分为模型组、电针组，每组各7只。取电针组大鼠“百会”及“大椎”穴，采用疏密波刺激30min，电流强度1～3mA，频率20Hz／80Hz，疏、密波交替时间各为1．5s。用实时荧光定量聚合酶链反应（RT—PCR）技术分别检测大鼠大脑皮层组织Bcl-2和BaxmRNA的表达。结果：与假手术组相比，模型组Bcl-2、BaxmRNA表达均显著升高，而Bcl-2／Bax比值显著下降；与模型组相比，电针组BaxmRNA表达降低，Bcl-2mRNA表达虽无统计学差异，但Bcl-2／Bax比值显著上升，形成以Bcl-2占优势的Bcl-2／Bax二聚体。结论：电针可以通过调控内源性凋亡途径，抑制Bax的促凋亡作用，降低缺血再灌注区的细胞凋亡，促进细胞的存活，这可能是电针拮抗局灶性脑缺血再灌注损伤后的神经细胞凋亡，保护脑神经元的分子生物学机制之一。

英文摘要：

Objective：To observe the effect of electro -acupuncture（EA） on the expression of Bcl -2 and Bax mRNA on ischemic cerebral neurons in rats with cerebral ischemia-reperfusion（CI/R）. Methods：A total of 21 healthy male Spragne- Dawley rats were randomized into sham operation group （SHAM group）, and focal cerebral ischemia operation group （n = 16 ）. A model of reversible middle cerebral artery occlusion in rat was proposed based on the modified classic Logna＇ s thread occlusion method （ right middle cerebral artery occlusion（MCAO） for 2 hours and reperfusion for 24 hours）. Ischemia model rats were divided into model group （CI/R group, n = 7 ）and model ＋ EA group（ C I/R ＋ EA group , n = 7 ）. EA（ disperse and dense waves,20 - 80Hz, 1 - 3 mA） was applied to＂ Dazhui＂ （ GV 14 ） and＂ Baihui＂ （ GV 20 ） for 30 minutes. The expression of Bcl - 2 and Bax mRNA in cerebral cortex were measured using real - time quantitative RT - PCR method. Results ： Compared with sham group, the expressions of Bcl - 2 and Bax mRNA in CI/R group were significantly increased, but the ratio of Bcl - 2 and Bax was obviously decreased ,while the expression of Bcl -2 mRNA in CI/R ＋ EA group was significantly increased. Compared with CI/R group ,the expression of Bax mRNA was decreased, the expression of Bcl -2 mRNA showed no significant changes ,while the ratio of Bcl - 2 and Bax was increased. And the Bcl - 2/Bax dipolymers dominated by Bcl - 2 were generated after EA treatment. Conclusion ： The result suggests that EA can adjust the endogenous apoptosis pathway,inhibit the apoptosis induced by Bax and decrease the apoptosis phenomenon in the isehemia reperfusion area, enhance the number of survival cells, and relieve the cerebral ischemia reperfusion injury. EA plays a satisfactory neuroprotective effect after focal cerebral ischemia reperfusion by inhibiting the apoptosis of neurons.