Zhou Wei, Chen Lei, Hu Xiqing, Cao Shanshan, Yang Junxiu
Department of Neurology, Tianjin United Medical Centre.
Tianjin Huanhu Hospital, Tianjin, China.
Neuroreport. 2019 Jan 16;30(2):60-65. doi: 10.1097/WNR.0000000000001149.
The aim of this study is to investigate the protective effect of epigallocatechin-3-gallate (EGCG) on apoptosis and mTOR/AKT/GSK-3β pathway in substantia nigra neurons in 6-dopamine-induced Parkinson rats. A total of 30 healthy male SD rats were randomly divided into control group, the Parkinson model group, and Parkinson model+EGCG treatment group. The model and EGCG groups were injected into the right striatum with 6-OHDA to establish the Parkinson model, and the control group was injected with saline only. The EGCG group was intragastrically administered with EGCG 50 mg/kg daily for 4 weeks. The rats' turns, speed, and left forelimb usage; neuron apoptosis by TUNEL; and the α-synuclein protein expression in substantia nigra by immunohistochemical staining were studied. Western blotting was used to detect the relative protein (mTOR, AKT and GSK-3β) expressions. Compared with the model group, the EGCG group significantly reduced the rotation speed; increased the left forelimb usage (P<0.01); reduced the neuron apoptosis (P<0.01); decreased α-synuclein expression (P<0.01); and decreased the mTOR, AKT, and GSK-3β protein expressions (P<0.01). EGCG can reduce neuron cell apoptosis in substantia nigra neurons in 6-OHDA-induced Parkinson rats. The mechanism might be related to mTOR/AKT/GSK-3β activation.
本研究旨在探讨表没食子儿茶素-3-没食子酸酯(EGCG)对6-羟基多巴胺诱导的帕金森病大鼠黑质神经元凋亡及mTOR/AKT/GSK-3β信号通路的保护作用。将30只健康雄性SD大鼠随机分为对照组、帕金森病模型组和帕金森病模型+EGCG治疗组。模型组和EGCG组经右侧纹状体注射6-羟基多巴胺建立帕金森病模型,对照组仅注射生理盐水。EGCG组每天灌胃给予50 mg/kg EGCG,持续4周。观察大鼠的旋转次数、速度和左前肢使用情况;采用TUNEL法检测神经元凋亡;通过免疫组织化学染色检测黑质中α-突触核蛋白的表达。采用蛋白质印迹法检测相关蛋白(mTOR、AKT和GSK-3β)的表达。与模型组相比,EGCG组显著降低了旋转速度;增加了左前肢使用次数(P<0.01);减少了神经元凋亡(P<0.01);降低了α-突触核蛋白表达(P<0.01);降低了mTOR、AKT和GSK-3β蛋白表达(P<0.01)。EGCG可减少6-羟基多巴胺诱导的帕金森病大鼠黑质神经元细胞凋亡。其机制可能与激活mTOR/AKT/GSK-3β信号通路有关。