3xTg-AD小鼠有氧和阻力训练后海马生长因子和肌细胞组织蛋白酶B的表达。

International Journal of Chronic Diseases Pub Date : 2020-01-30 eCollection Date: 2020-01-01 DOI:10.1155/2020/5919501
Gabriel S Pena, Hector G Paez, Trevor K Johnson, Jessica L Halle, Joseph P Carzoli, Nishant P Visavadiya, Michael C Zourdos, Michael A Whitehurst, Andy V Khamoui
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引用次数: 17

摘要

有氧训练(AT)可以支持阿尔茨海默病(AD)患者的大脑健康;然而,阻力训练(RT)在AD中的作用尚未得到很好的确定。除了对大脑的直接影响外,运动还可以通过分泌肌肉来源的肌肉因子来调节大脑功能。目标本研究检测了AT和RT对三转基因(3xTg-AD) AD模型海马BDNF和IGF-1信号、β-淀粉样蛋白表达和肌细胞组织蛋白酶B的影响。3xTg-AD小鼠被分配到以下组之一:久坐(Tg),有氧训练(Tg+AT, 9周跑步机)或阻力训练(Tg+RT, 9周加权爬梯)(n = 10/组)。在训练前和训练后评估旋转杆潜伏期和力量。训练后收集海马和骨骼肌,并通过高分辨率呼吸仪、ELISA和免疫印迹进行分析。训练后Tg+RT组握力高于Tg和Tg+AT组(p < 0.01)。只有Tg+AT能改善旋转杆峰潜伏期(p < 0.01)。Tg+AT组和Tg+RT组海马IGF-1浓度较Tg组高15% (p < 0.05);然而,p-IGF-1R、p-Akt、p-MAPK和p-GSK3β的下游信号没有改变。组织蛋白酶B、海马p- creb和BDNF以及海马线粒体呼吸均不受AT和RT的影响,Tg+RT组β-淀粉样蛋白比Tg组降低约30% (p < 0.05)。这一数据表明,有规律的抗阻训练可以减少海马体内的β-淀粉样蛋白,同时增加IGF-1的浓度。这两种类型的训练都有不同的好处,要么是通过改善身体机能,要么是通过改变海马体中的信号。因此,包括这两种训练方式可以解决中枢缺陷,以及AD的周边合并症。
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Hippocampal Growth Factor and Myokine Cathepsin B Expression following Aerobic and Resistance Training in 3xTg-AD Mice.

Aerobic training (AT) can support brain health in Alzheimer's disease (AD); however, the role of resistance training (RT) in AD is not well established. Aside from direct effects on the brain, exercise may also regulate brain function through secretion of muscle-derived myokines. Aims. This study examined the effects of AT and RT on hippocampal BDNF and IGF-1 signaling, β-amyloid expression, and myokine cathepsin B in the triple transgenic (3xTg-AD) model of AD. 3xTg-AD mice were assigned to one of the following groups: sedentary (Tg), aerobic trained (Tg+AT, 9 wks treadmill running), or resistance trained (Tg+RT, 9 wks weighted ladder climbing) (n = 10/group). Rotarod latency and strength were assessed pre- and posttraining. Hippocampus and skeletal muscle were collected after training and analyzed by high-resolution respirometry, ELISA, and immunoblotting. Tg+RT showed greater grip strength than Tg and Tg+AT at posttraining (p < 0.01). Only Tg+AT improved rotarod peak latency (p < 0.01). Hippocampal IGF-1 concentration was ~15% greater in Tg+AT and Tg+RT compared to Tg (p < 0.05); however, downstream signals of p-IGF-1R, p-Akt, p-MAPK, and p-GSK3β were not altered. Cathepsin B, hippocampal p-CREB and BDNF, and hippocampal mitochondrial respiration were not affected by AT or RT. β-Amyloid was ~30% lower in Tg+RT compared to Tg (p < 0.05). This data suggests that regular resistance training reduces β-amyloid in the hippocampus concurrent with increased concentrations of IGF-1. Both types of training offered distinct benefits, either by improving physical function or by modifying signals in the hippocampus. Therefore, inclusion of both training modalities may address central defects, as well as peripheral comorbidities in AD.

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