表没食子儿茶素没食子酸酯对D-半乳糖诱导的AD模型小鼠Aβ生成作用的研究  

Study on Generating Effect of EGCG on Aβ of Model Mice with Alzheimer's Disease Induced by D-galactose

作　　者：王会敏[1] 何柯新 尚陈宇 刘冬冬[1] 徐建华[1] WANG Huimin;HE Kexin;SHANG Chenyu;LIU Dongdong;XU Jianhua

机构地区：[1]广东省中医院二沙岛分院,广东广州510130 [2]广州市惠爱医院,广东广州510370

出　　处：《新中医》2018年第9期17-21,共5页New Chinese Medicine

基　　金：广东省中医药局科研项目(20161092)

摘　　要：目的:探讨表没食子儿茶素没食子酸酯(Epigallocatechin-3-gallate,EGCG)对D-半乳糖诱导的阿尔茨海默病(Alzheimer’s disease,AD)模型小鼠β淀粉样肽(Amyloid-βpeptide,Aβ)生成作用的影响。方法:将60只昆明小鼠随机分为对照组、模型组、VE阳性组、EGCG低剂量组、EGCG中剂量组、EGCG高剂量组,每组10只。注射D-半乳糖建立AD小鼠模型后,对照组和模型组灌胃等量双蒸水;VE阳性组每天灌胃5.6%VE 1次;EGCG低、中、高剂量组分别按每天2 mg/kg灌胃0.04%EGCG、4 mg/kg灌胃0.08%EGCG和6 mg/kg灌胃0.12%EGCG 1次;持续给药28天后通过避暗试验和Morris水迷宫试验观察小鼠动物行为学变化;ELISA法检测小鼠脑匀浆中白细胞介素-2(IL-2)、白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)和Aβ水平;苏木精-伊红(HE)染色观察海马内神经元的变化。结果:EGCG能明显延长AD模型小鼠跳台潜伏期、减少跳台错误次数、缩短通过迷宫的时间和减少进入盲端的错误次数;且能显著减轻D-半乳糖诱导的AD模型小鼠海马神经元的损伤及降低其脑内IL-6、TNF-α和Aβ表达水平,差异均有统计学意义(P<0.05)。结论:EGCG可能通过降低D-半乳糖诱导的AD模型小鼠脑内Aβ的含量,来抑制神经细胞凋亡,从而改善学习记忆障碍。Objective：To explore the generating effect of epigallocatechin-3-gallate（EGCG） on amyloid-β peptide（Aβ） of model mice with Alzheimer＇s disease（AD） induced by D-galactose. Methods： Divided 60 cases of mice from Kunming randomly into the control group, the model group, the VE positive group, the EGCG groups of low, middle and high dose, 10 cases in each group.After establishing the model mice with AD by injection of D-galactose, the control group and the model group were given equivalent double distilled water by gavage. The VE positive group was given 5.6% VE by gavage once a day. The EGCG groups of low,middle and high dose were respectively given 2 mg/kg 0.04% EGCG,4 mg/kg 0.08% EGCG,6 mg/kg 0.12% EGCG by gavage once a day. After continuously treating for 28 days, observed the changes of animal behaviors by the step-through test and Morris water maze test,detected levels of interleukins-2（IL-2）,interleukins-6（IL-6）,tumor necrosis factor-α（TNF-α） and Aβ in brain homogenate of mice by ELISA method, and observed the changes of neurons in hippocampus of mice by hematoxylin-eosin staining. Results： EGCG can obviously prolong the step-down latency,reduce the error frequency of step-down,shorten the passing time through maze and reduce the error frequency of entering dead end of the model mice with AD,and it can obviously relieve the injury of neurons in hippocampus of model mice with AD induced by D-galactose and reduce the expression levels of IL-6, TNF-α and Aβ, differences being significant（P〈0.05）. Conclusion：EGCG possibly can inhibit the apoptosis of neurons by reducing the content of Aβ of bain in the model mice with AD induced by D-galactose,so as to improve the learning and memory impairment.

关 键 词：阿尔茨海默病(AD) 表没食子儿茶素没食子酸酯(EGCG) β淀粉样肽(Aβ) 动物实验 小鼠 

分 类 号：R285.5[医药卫生—中药学]