运动功能障碍是缺血性脑卒中的主要症状，与神经血管单元（NVU）稳态紧密相关。Cx43 ser368位点磷酸化是维持NVU稳态的关键，miR-181b/PKC信号轴可促进Cx43ser368位点磷酸化修饰。巨刺法改善缺血性脑卒中后运动障碍疗效确切，我们前期研究发现巨刺法可提高MCAO模型鼠白质PKC蛋白浓度，上调NVU重要组份星形胶质细胞表达，但机制不清。故本项目以miR-181b/PKC轴调控Cx43ser368磷酸化参与维持NVU稳态为切入点，对MCAO模型鼠进行巨刺干预，观察运动行为改变，DTI追踪白质神经纤维束变化，取双侧脑白质，激光共聚焦观察神经元、小胶质细胞、星型胶质细胞、内皮细胞表达改变，Western blot检测APQ4、ZO-1、occludin蛋白变化，实时荧光定量检测miR-181b表达水平，ELISA检测PKC浓度变化，阐明巨刺改善缺血性脑卒中后运动障碍的作用机制。

Motor dysfunction is a major symptom of ischemic cerebral apoplexy, which is closely related to the homeostasis of neural vascular unit (NVU). The phosphorylation of Cx43ser368 sites is the key to the maintain the homeostasis of NVU, miR-181b/PKC signal axis can promote phosphorylated modification of Cx43ser368 site. Opposing needling have curative effect to improve motor dysfunction after ischemic stroke, previous study found Opposing needling can improve PKC protein concentration in white matter of the MCAO rat, increase the expression of astrocytes marker which were the NVU important components, but the mechanism was unclear. This study on the basis of the homeostasis of NVU modulated by miR-181b/PKC axis targeted Cx43ser368 phosphorylation, opposing needling will be adopted to treat MCAO rats, to observe the exercise behavior changes, DTI tracked white matter changes in nerve fiber bundles, then take the bilateral white matter, laser confocal observation the express changes with neurons and microglia, radial glial cells and endothelial cells, Western blot will be used to detect the changes of proteins(APQ4, ZO-1, occludin), Real-time fluorescence quantitative to test miR-181b expression level, ELISA to detect concentration changes of PKC, so as to clarify the mechanism of opposing needling in improving motor dysfunction after ischemic stroke.