电针治疗对急性缺血性脑梗死大鼠树突棘可塑性的影响

The effects of electroacupuncture on dendritic spine plasticity in rats with acute ischemic cerebral infarction

目的探讨电针治疗对急性缺血性脑梗死大鼠树突棘可塑性的影响。方法共选取SPF级雄性SD大鼠90只，将其随机分为假手术组、MCAO组及电针治疗组。MCAO组及电针治疗组大鼠采用热凝法制作大鼠大脑中动脉局灶性脑缺血模型，于脑缺血1周、2周及4周时观察各组实验大鼠脑缺血区皮质锥体神经元树突棘密度和Ephrin-A5表达的变化情况。结果各组实验大鼠树突棘大多呈蘑菇状，电针治疗组则出现较多蚓状树突棘。MCAO组与假手术组比较，前者树突棘密度于术后1周时明显降低，在术后2周、4周时进一步降低（P〈0．01）；电针治疗组与假手术组比较，前者树突棘密度在治疗1周后明显升高（P〈0．01），并持续至治疗后4周时；Ephrin．A5主要分布于脑皮质神经元胞浆中；MCAO组与假手术组比较，前者Ephrln-A5 mRNA表达在术后1周时明显增高，至少持续到术后4周时，并且在术后2周时Ephrin—A5mRNA表达水平达到峰值（P〈0．01）；电针治疗组与假手术组比较，前者Ephrin-A5 mRNA表达水平于治疗后1周时明显增高，随后出现下降趋势，于治疗后4周时Ephrin-A5mRNA表达水平达到最低值（P〈0．01），接近于假手术组水平。结论电针刺激能促进脑梗死实验大鼠神经功能恢复，其中一个重要可能机制是电针刺激能调节Ephrin-A5表达，从而促进神经树突棘可塑性，加快受损神经功能恢复。

Objective To investigate the effects of electroacupuncture（ EA ） on dendritic spine plasticity after acute ischemic cerebral infarction in rats. Methods A total of 90 SPF male Sprague-Dawley rats were divided into a sham operation （SO） group, a MCAO group, and an EA treatment （ET） group. MCAO model was established with heat-coagulation method. At the end of 1, 2 and 4 weeks after MCAO or EA treatment, the changes of the dendritic spine density, expression patterns of Ephrin-A5 were observed. Results Generally the dendritic spine shape was mushroom-like in all the groups, while in ET group showed some earthworm-like spines. Compared to SO group, the dendritic spine density in the MCAO group significantly decreased 1 week after operation, and Lnore lower at the end of 2 and 4 weeks after operation （P 〈 0.01 ）. Moreover, the dendritic spine density was increased at the end of 1 week and lasted till the end of 4 weeks after EA treatment （P 〈 0.01 ）. The signal from Ephrin-A5 was detected mainly in neuron kytoplasm. Compared to SO group, Ephrin-A5 mRNA in MCAO group significantly increased at the end of the 1st week after operation, and reached peak value after 2 weeks （P 〈 0.01 ）. It was also shown that the Ephrin-A5 mRNA was significantly upregulated at the end of 1 week after EA treatment, and then kept downtrend along the next 3 weeks, and reached valley value close to SO group at the 4th week after EA treatment （P 〈0.01 ）. Conclusion EA treatment can facilitate neural function recovery, which may attribute to the improved dendritic spine plasticity and the regulated expression of Ephrin-A5 in the peri-infarct cerebral cortex.