目的 探讨电针对帕金森病（PD）小鼠黑质中胰高血糖样肽⁃1受体（GLP⁃1R）介导的磷脂酰肌醇 3⁃激酶（PI3K）/蛋白激酶 B（AKT）/糖原合酶激酶⁃3β（GSK⁃3β）通路的作用机制。方法 将 48 只 C57/BL6 小 鼠随机分为正常组（NC）、模型组（M）、电针组（EA）、抑制剂组（DI），各12只。本研究采用鱼藤酮灌胃4周制 备 PD 小鼠模型。采用敞箱实验测定行为学变化，采用免疫组化法检测黑质酪氨酸轻化酶（TH）水平，采用 Western blot检测黑质GLP⁃1R、PI3K、AKT和GSK⁃3β蛋白表达水平。结果 EA和DI干预均可有效改善PD小 鼠各项行为学指标（均P < 0.05）、升高黑质TH水平（均P < 0.01）、上调GLP⁃1R、PI3K、AKT及下调GSK⁃3β蛋白表 达水平（均P < 0.01）。结论 电针可能通过调控GLP⁃1R介导的PI3K/AKT/GSK⁃3β通路在PD中发挥保护机制。

Objective To investigate the mechanism of electroacupuncture（EA）in the regulation of the phosphatidylinositol 3⁃kinase（PI3K）/ protein kinase B（AKT）/ glycogen synthase kinase⁃3β（GSK⁃3β）signaling pathway mediated by glucagon ⁃like peptide ⁃1 receptor（GLP ⁃1R）in the substantia nigra（SN）of mice with Parkinson′s disease（PD）. Methods Forty⁃eight C57/BL6 mice were randomly divided into normal group（NC）， model group（M），EA group（EA）and DPP⁃4 inhibitor group（DI），with 12 mice in each group. The behavioral changes were determined by the open field test. The level of tyrosine hydroxylase（TH）in the SN was determined by immunohistochemistry. The expression levels of GLP⁃1R，PI3K，AKT and GSK⁃3β in the SN were detected by Western blot. Results Both EA and DPR⁃4 inhibitor effectively improved the behavioral indexes of PD mice（all P < 0.05），increased the TH level in the SN（all P < 0.01），up ⁃ regulated the expression levels of GLP ⁃ 1R， PI3K，AKT and down⁃regulated the expression level of GSK⁃3β（all P < 0.01）. Conclusions EA may play a pro⁃ tective role in PD by regulating the GLP⁃1R⁃mediated PI3K/ Akt /GSK⁃3β signaling pathway.