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当代阿耳茨海默病研究

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ISSN (Print): 1567-2050
ISSN (Online): 1875-5828

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Research Article

高强度间歇训练在阿尔茨海默病大鼠模型中预防认知障碍并增加肌肉基因FNDC5和PPARGC1A的表达

卷 19, 期 12, 2022

发表于: 30 December, 2022

页: [830 - 840] 页: 11

弟呕挨: 10.2174/1567205020666221207103109

价格: $65

摘要

背景：阿尔茨海默病是世界上最常见的神经退行性疾病，以神经元结构和功能的进行性丧失为特征，其主要组织病理学标志是脑内β-淀粉样蛋白的积累。 目的：众所周知，运动是一种神经保护因素，肌肉产生和释放肌肉因子，在炎症和代谢功能障碍中发挥内分泌作用。因此，本研究旨在通过长期HIIT训练与注射β淀粉样蛋白1-42引起的阿尔茨海默氏症模型认知损伤建立运动益处之间的关系。 方法：为此，48只雄性Wistar大鼠被分为四组:久坐假组(SS)、训练假组(ST)、久坐阿兹海默症组(AS)和训练阿兹海默症组(AT)。动物接受立体定向手术，并接受a β1-42或生理盐水的海马注射。术后7天，12天的跑步机适应，随后进行5次最大跑步测试(MRT)和55天的HIIT，大鼠进行莫里斯水迷宫测试。然后对动物实施安乐死，提取腓肠肌组织，通过qRT-PCR分析Fibronectin type III domain containing 5 (FNDC5)、PPARG Coactivator 1 Alpha (PPARGC1A)和Integrin subunit beta 5 (ITGB5-R)的表达以及横截面积。 结果：HIIT可防止淀粉样蛋白β1-42输入引起的认知缺陷(p < 0.0001)，引起肌纤维的适应(p < 0.0001)，调节FNDC5 (p < 0.01)、ITGB5 (p < 0.01)和PPARGC1A (p < 0.01)的基因表达，并诱导FNDC5外周蛋白表达的增加(p < 0.005)。 结论：因此，我们得出结论，HIIT可以预防Aβ1-42输注引起的认知损伤，构成一种调节重要遗传和蛋白质途径的非药物工具。

关键词: 阿尔茨海默病，鸢尾素，运动，HIIT, Aβ1-42, FNDC5, PPARGC1A。

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