Study on Generating Effect of EGCG on Aβof Model Mice with Alzheimer's Disease Induced by D-galactose
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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2mg/kg灌胃0.04%EGCG、4mg/kg灌胃0.08%EGCG和6mg/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。
Abstract:
Objective:To explore the generating effect of epigallocatechin-3-gallate(EGCG)on amyloid-β peptide(Aβ )of modelmice with Alzheimer's disease(AD)induced by D-galactose.Methods:Divided 60 cases of mice from Kunmingrandomly 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 modelmice with AD by injection of D-galactose,the control group and the model group were given equivalent double distilled w ater 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 2m g/kg 0.04%EGCG,4m g/kg 0.08%EGCG,6m g/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 w ater m aze test, detected levels of interleukins-2(IL-2), interleukins-6(IL-6),tumor necrosis factor-α (TNF-α )and Aβ in brain homogenate ofmice by ELISA method,and observed the changes of neurons in hippocampus of mice by hem atoxylin-eosin staining.Results:EGCG can obviously prolong the step-dow n latency,reduce the error frequency of step-dow n,shorten the passing time through m aze and reduce the error frequency of entering dead end of the modelmice 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 modelmice with AD induced by D-galactose,so as to improve the learning and memory impairment.