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首页> 外文期刊>International Journal of Chronic Diseases >Hippocampal Growth Factor and Myokine Cathepsin B Expression following Aerobic and Resistance Training in 3xTg-AD Mice
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Hippocampal Growth Factor and Myokine Cathepsin B Expression following Aerobic and Resistance Training in 3xTg-AD Mice

机译：在3XTG-AD小鼠中有氧和抗性训练后的海马生长因子和肌球蛋白组织蛋白酶B表达

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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 (p0.01). Only Tg+AT improved rotarod peak latency (p0.01). Hippocampal IGF-1 concentration was ~15% greater in Tg+AT and Tg+RT compared to Tg (p0.05); 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 (p0.05). 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.
机译：有氧训练（AT）可以支持阿尔茨海默病（广告）的大脑健康;然而，广告中的阻力训练（RT）的作用并不明确。除了对大脑的直接影响，运动还可以通过分泌肌肉衍生的肌电管来调节脑功能。目标。该研究检测了在AD的三重转基因（3XTG-AD）模型中的海马BDNF和IGF-1信号，β-淀粉样蛋白表达和肌肌内膜蛋白酶B的效果。将3XTG-AD小鼠分配给以下组中的一种：久坐不动（TG），有氧培训（TG + AT，9？WKS跑步机运行），或耐受培训（TG + RT，9？WKS加权梯爬）（n = 10 /组）。评估rotarod延迟和强度进行预先和接受。在训练后收集海马和骨骼肌，并通过高分辨率呼​​吸测定法，ELISA和免疫印迹分析。 TG + RT在接受情况下显示比Tg和Tg +更大的抓握强度（P <0.01）。仅TG +改进旋转峰值梯度（P <0.01）。与Tg相比，海马IGF-1浓度在TG + AT和TG + RT中〜15％较高（P <0.05）;然而，P-IGF-1R，P-AKT，P-MAPK和P-GSK3β的下游信号未被改变。组织蛋白酶B，海马P-CREB和BDNF，以及海马线粒体呼吸不受AT或RT的影响。与Tg相比，β-淀粉蛋白在Tg + Rt中〜30％（P <0.05）。该数据表明，具有较高的IGF-1浓度的常规阻力训练在海马同时降低β-淀粉样蛋白。通过改善物理功能或通过在海马中修改信号，两种类型的培训都提供了明显的好处。因此，包含训练方式可以解决中央缺陷，以及广告中的外周可用性。

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