Yin Ting, Chen Hai-Ping, Wang Wen, Zhang Wei, Huang Juan
Second Ward of Department of Rehabilitation, China Resources Wuhan Iron-steel Corporation General Hospital, Wuhan 430080, China.
Department of Neurology, Henan Provincial People's Hospital, Zhengzhou 450000.
Zhen Ci Yan Jiu. 2019 Jul 25;44(7):497-500. doi: 10.13702/j.1000-0607.190067.
To observe the effect of electroacupuncture (EA) on expression of cerebral Cx43 protein in acute cerebral infarction (ACI) rats so as to explore its mechanisms underlying improvement of ACI.
Sixty male SD rats were randomly divided into sham operation, model and EA preconditioning groups (＝20 in each group). Fourteen days before modeling, the rats in the EA preconditioning group accepted EA stimulation (3 Hz/15 Hz, 1 mA) at Dingzhongxian (MS5) and Dingpangxian (MS8) for 30 min, once daily, 6 times a week for 2 weeks. The ACI model was established by occlusion of the middle cerebral artery for 120 min, followed by reperfusion. Twenty-four hours after modeling, the neurological function was evaluated according to the Zea-Longa's score criteria. The triphenyltetrazolium chloride (TTC) staining method was used to detect the cerebral infarct volume. The expression levels of Cx43, phosphorylated (p)-Cx43 and PKC proteins in the right cerebral cortical infarction region were detected by Western blot.
The neurological function scores and the infarct volume were significantly higher in the model group than those in the sham operation group (<0.05), and obviously lower in the EA preconditioning group than in the model group (<0.05). The expression level of cerebral Cx43 protein was significantly increased (<0.05), and those of p-Cx43 and PKC proteins were notably decreased in the model group relevant to the sham operation group (<0.05). In the EA preconditioning group, the expression level of Cx43 was significantly decreased and those of p-Cx43 and PKC proteins were significantly increased than those in the model group (<0.05).
EA pretreatment can relieve neurological damage and reduce cerebral infarction volume in ACI rats, which may be related to its function in promoting Cx43 protein phosphorylation via up-regulating PKC expression in the ischemic cerebral region.
观察电针（EA）对急性脑梗死（ACI）大鼠脑Cx43蛋白表达的影响，以探讨其改善ACI的机制。
将60只雄性SD大鼠随机分为假手术组、模型组和EA预处理组（每组20只）。建模前14天，EA预处理组大鼠于顶中线（MS5）和顶旁线（MS8）接受EA刺激（3Hz/15Hz，1mA）30分钟，每日1次，每周6次，共2周。采用大脑中动脉闭塞120分钟后再灌注的方法建立ACI模型。建模后24小时，根据Zea-Longa评分标准评估神经功能。采用氯化三苯基四氮唑（TTC）染色法检测脑梗死体积。通过蛋白质免疫印迹法检测右侧大脑皮质梗死区域Cx43、磷酸化（p）-Cx43和蛋白激酶C（PKC）蛋白的表达水平。
模型组神经功能评分和梗死体积均显著高于假手术组（P<0.05），而EA预处理组明显低于模型组（P<0.05）。与假手术组相比，模型组脑Cx43蛋白表达水平显著升高（P<0.05），p-Cx43和PKC蛋白表达水平显著降低（P<0.05）。与模型组相比，EA预处理组Cx43表达水平显著降低，p-Cx43和PKC蛋白表达水平显著升高（P<0.05）。
EA预处理可减轻ACI大鼠神经损伤，减小脑梗死体积，其机制可能与上调缺血脑区PKC表达，促进Cx43蛋白磷酸化有关。
