电针刺激对局灶性脑梗死大鼠梗死灶周围皮质ROCK1与ROCK2表达的影响

目的 观察电针刺激对局灶性脑梗死大鼠神经功能及梗死灶周围皮质ROCK1和ROCK2表达的影响，初步探讨其对大脑缺血组织的保护机制。方法 将40只雄性SD大鼠随机分为正常组、假手术组、模型组和电针穴位组，每组10只。用改良Longa法制作大脑中动脉闭塞（MCAO）模型，在大鼠麻醉苏醒后90 min对电针穴位组大鼠进行电针刺激，每天1次，连续14 d。分别在术后1、3、7、14 d时对各组大鼠进行改良神经功能缺损评分（mNSS）。术后14 d时，用免疫组化和蛋白质印迹法检测缺血侧大脑皮质中ROCK1、ROCK2蛋白的表达情况。结果 正常组和假手术组未出现神经功能缺损表现。术后7、14 d，电针穴位组mNSS评分较模型组下降（P<0.05）。免疫组化和免疫印迹结果显示，模型组ROCK1和ROCK2蛋白表达上调，电针穴位组ROCK1和ROCK2蛋白表达较模型组减少（P<0.05）。结论 电针刺激促进局灶性脑梗死后大鼠神经功能恢复，可能与其下调ROCK1和ROCK2蛋白表达有关。

Effect of electroacupuncture on ROCK1 and ROCK2 expression in rat peri-infarct cortex after focal cerebral infarction

Objective To observe the effect of electroacupuncture (EA) intervention on the expression of Rho-associated kinase 1(ROCK1) and Rho-associated kinase 2 (ROCK2) in rat peri-infarct cortex after middle cerebral artery occlusion (MCAO), so as to study the underlying mechanism by which EA improves cerebral ischemia. Methods Totally 40 male Sprague Dawley (SD) rats were equally randomized into four groups, control group, sham-operation group, model group and EA group. MACO in the model group and EA group was successfully established by an improved Longa procedure. EA was given 90 min after resuscitation for the EA group, once a day for 14 days. The modified neurological severity scores (mNSS) of rats in each group were determined on the 1^st day, 3^rd day, 7^th day and the 14^th day after operation. Immunohistochemistry and Western blotting analysis were used to detect the expression of ROCK1 and ROCK2 in the brain 14 d after operation. Results Neural dysfunction was not observed in the control group and sham-operation group. The values of mNSS were significantly different between model group and EA group at 7 d, 14 d after operation (P<0.05). Both immunohistochemical staining and Western blotting analysis indicated that the expression levels of ROCK1 and ROCK2 were up-regulated in model group, while those in EA group were significantly less than those in the model group (P<0.05). Conclusion The expression of ROCK1 and ROCK2 is up-regulated in rat cortex after focal cerebral infarction, and the up-regulation can be prevented by EA intervention, which might be one of the mechanisms by which EA promotes the recovery of neurological dysfunction after cerebral infarction.