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张子怡,康伟民,张 晟,薄 海.高强度间歇运动训练上调APP/PS1转基因阿尔兹海默病小鼠海马线粒体自噬的研究[J].中国康复医学杂志,2020,(6):670~675
高强度间歇运动训练上调APP/PS1转基因阿尔兹海默病小鼠海马线粒体自噬的研究    点此下载全文
张子怡  康伟民  张 晟  薄 海
天津体育学院天津市运动生理学与运动医学重点实验室,天津,300381
基金项目:国家自然科学基金项目(31110103919,31571224);天津市教委科研计划项目(2018KJ233);武警后勤学院研究基金项目(WHJ201714)
DOI:10.3969/j.issn.1001-1242.2020.06.005
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摘要:
      摘要 目的:观察高强度间歇运动训练干预是否能改善APP/PS1转基因AD小鼠病理表现,并探讨线粒体自噬在其间的生物学效应。 方法:8月龄雄性APP/PS1转基因小鼠分为转基因模型安静组(SED-Tg)和转基因模型+高强度间歇运动训练组(HIIT-Tg),C57BL/6 野生型小鼠纳入野生型安静组(SED-Wt)。HIIT-Tg组动物进行12周高强度间歇运动训练。避暗被动回避实验检测学习记忆能力,JC-1荧光探针检测海马线粒体膜电位,二氯荧光素探针检测海马线粒体ROS,Western Blot法检测脑海马Aβ-42、BDNF、AMPK、PINK1、Parkin、Bnip3蛋白表达。 结果:①SED-Tg组与SED-Wt组比较,逃避潜伏期、线粒体膜电位、BDNF、AMPK、PINK1、Parkin和Bnip3蛋白表达显著降低(P<0.05—0.01),线粒体ROS产生速率和Aβ-42蛋白表达显著升高(P<0.01)。②HIIT-Tg组与SED-Tg组比较,逃避潜伏期、线粒体膜电位、BDNF、AMPK、PINK1和Parkin蛋白表达显著升高(P<0.01),线粒体ROS产生速率和Aβ-42蛋白表达显著降低(P<0.01)。 结论:高强度间歇运动训练可通过上调AMPK- PINK1/Parkin介导的线粒体自噬,改善线粒体功能,减少APP/PS1转基因AD小鼠脑海马Aβ积聚,提高记忆和学习能力。
关键词:APP/PS1转基因鼠  阿尔兹海默病  高强度间歇运动训练  线粒体自噬  脑海马
High-intensity interval training-induced neuroprotection of hippocampus in APP/PS1 transgenic mice via upregulation of mitophagy    Download Fulltext
Tianjin Key Laboratory of Exercise Physiology and Sports Medicine, Tianjin University of sport, Tianjin, 300381
Fund Project:
Abstract:
      Abstract Objective: To observe the effect of high-intensity interval training on hippocampus in APP/PS1 transgenic mice, as well as the role of mitophagy. Method: Male 8-month APP/PS1 transgenic mice were divided into two groups: sedentary APP/PS1 transgenic mice group (SED-Tg), and high-intensity interval training APP/PS1 transgenic mice group (HIIT-Tg). C57BL/6 wile-type mice were placed in sedentary wild type mice group (SED-Wt). HIIT-Tg mice were subjected to a high-intensity interval training for 12 weeks. Learning ability and memory were evaluated by passive avoidance test. Mitochondrial membrane potential was measured by JC-1 probe. Mitochondrial ROS production was monitored using the dichlorofluorescin diacetate. The protein expressions of Aβ-42, BDNF, AMPK, PINK1, Parkin and Bnip3 were detected by western blotting. Result: ①Comparing with SED-Wt group, the retention latency time, membrane potential, protein expressions of BDNF, AMPK, PINK1, Parkin and Bnip3 showed dramatic decrease in SED-Tg group(P<0.05—0.01), while ROS production and Aβ-42 level increased significantly (P<0.01). ②Comparing with SED-Tg group,the retention latency time, membrane potential, protein expressions of BDNF, AMPK, PINK1 and Parkin showed dramatic increase in HIIT-Tg group (P<0.01), while ROS production and Aβ-42 level decreased significantly (P<0.01). Conclusion: High-intensity interval training could enhance AMPK -PINK1/Parkin -mediated mitophagy, which in turn ameliorate mitochondrial dysfunction, Aβ deposition and cognitive impairment in hippocampus of APP/PS1 transgenic mice.
Keywords:APP/PS1 transgenic mice  Alzheimer's disease  high-intensity interval training  mitophagy  hippocampus
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