关键词: 帕金森病,  , 电针,  , 酪氨酸轻化酶,  , 胰高血糖样肽?1受体

Abstract:

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. 

Key words:

Parkinson′s disease, electroacupuncture, tyrosine hydroxylase, glucagon?like peptide? 1 receptor