运动干预对阿尔茨海默病模型大鼠记忆能力及神经元AMPK信号分子和自噬的影响  

Effect of exercise intervention on Alzheimer's disease model and memory and neuron of rat AMPK signaling molecules and autophagy

作　　者：郭春阳[1] 刘涛[2] 李明[1] 

机构地区：[1]河南大学学生体质健康研究所,河南开封475001 [2]西安体育学院健康科学系,西安710068

出　　处：《河南大学学报（医学版）》2016年第3期182-188,共7页Journal of Henan University:Medical Science

基　　金：陕西省教育厅自然科学研究计划项目(2013JK0777)

摘　　要：〔目的〕探讨运动干预对阿尔茨海默病模型大鼠记忆能力及神经元AMPK信号分子和自噬的影响。〔方法〕将60只雄性SD大鼠随机分为正常对照组、运动对照组、AD模型对照组、AD模型训练组。在立体定位仪下向大鼠两侧海马注射Aβ25-35制造AD模型。实验结束后,通过Morris水迷宫检测各组大鼠学习记忆能力,用Nissl法检测海马神经元存活状态;通过免疫荧光染色检测磷酸化AMPK表达;用Western blot法检测P-AMPK、LC3I、LC3II及Beclin-1的表达。〔结果〕与AD模型对照组相比较,AD模型训练组大鼠的逃避潜伏期明显减少,穿越平台区域次数明显增加(P<0.01);AD模型训练组大鼠的CAI区海马神经元形态较AD模型对照组改善明显,神经元数目显著增加(P<0.05);P-AMPK在AD模型训练组大鼠的表达明显增强,且主要在胞浆表达;与AD模型对照组相比,AD模型训练组大鼠的P-AMPK和Beclin-1的蛋白表达都明显增强(P<0.01),LC3II/LC3I比值明显增加(P<0.01)。〔结论〕8周的跑台运动可明显改善AD模型大鼠的记忆能力、减少AD模型大鼠海马CAI区神经元损伤数量。其机制可能是8周运动训练激活AD模型大鼠海马神经元AMPK通路和自噬,进而保护神经元。〔Objective〕To investigate the effects of exercise intervention on Alzheimer＇s disease model and memory and neuron of rat AMPK signaling molecules and autophagy.〔Methods〕60 male SD rats were randomly divided into normal control group,exercise group, AD control group, AD training group. Model of rathippocampus to bilateral injection of Aβ25-35 manufacturing AD under stereotactic instrument. After the experiment through the test of Morris water maze learning and memory ability of rats in each group, the Nissle method for the detection of hippocampal neuron survival; immunofluorescent staining was used to detect the expression of phosphorylated AMPK expression; Western blot method to detect P-AMPK, LC3 I, LC3 II and Beclin-1.〔Results〕Compared with AD control group, AD training group escape latency of rats increased significantly, space exploration results significantly decreased, the decrease in the number of surviving neurons in hippocampus, the expression of P-AMPK and Beclin-1 decreased, but the ratio of LC3 II / LC3 I had no change; Compared with AD control group, the rats of AD training group behavior index were significantly improved, a marked increase in the number of hippocampal neuron survival the expression of PAMPK, LC3 II / LC3 I, Beclin-1 and ratios were significantly increased. 〔Conclusion〕8 weeks of treadmill exercise can improve the memory ability of AD rats, reduce the number of neurons in CAI area of hippocampus injury in rats AD model. The mechanism may be the expression of exercise training for 8 weeks to activate AD neurons of rat in the phosphorylation of AMPK,then cause neuronal autophagy to protect normal neurons.

关 键 词：腺苷酸活化蛋白激酶 阿尔茨海默病 自噬 运动 

分 类 号：R339.1[医药卫生—人体生理学]