Moderate Exercise Improves Experimental Cancer Cachexia by Modulating the Redox Homeostasis
Moderate Exercise Improves Experimental Cancer Cachexia by Modulating the Redox Homeostasis
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DOI：
10.3390/cancers11030285
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发表时间：
2019-03-01
期刊：
影响因子：
5.2
通讯作者：
Costelli, Paola
中科院分区：
文献类型：
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作者：
Ballaro, Riccardo;Penna, Fabio;Costelli, Paola
恶病质是一种使癌症患者管理复杂化的衰弱综合征。肌肉萎缩是恶病质的主要特征之一，与蛋白质降解途径的过度活化和线粒体功能的改变有关，这两者都可能是由氧化还原稳态受损引起的。本研究的目的是探讨在存在或不存在适度运动训练的情况下，氧化应激对癌症引起的恶病质的贡献。使用了携带结肠C26癌的小鼠，无论是久坐还是运动。前者表现出肌肉萎缩和氧化还原失衡，激活了抗氧化反应，上调了蛋白酶体依赖性蛋白质降解和自噬的标志物。适度的运动能够缓解肌肉萎缩并防止肌肉力量的丧失;这种模式与活性氧（ROS），羰基化蛋白和自噬标记物水平的降低以及抗氧化能力的提高有关。久坐不动的肿瘤宿主的肌肉也表现出线粒体自噬的分子标记物水平升高和线粒体质量降低。相反，C26宿主的运动导致线粒体质量增加。总之，适度的运动可能是一种有效的非药物方法，以防止癌症患者的肌肉萎缩，减少肌肉蛋白质catalysts和氧化应激和保护线粒体。
Cachexia is a debilitating syndrome that complicates the management of cancer patients. Muscle wasting, one of the main features of cachexia, is associated with hyper-activation of protein degradative pathways and altered mitochondrial function that could both result from impaired redox homeostasis. This study aimed to investigate the contribution of oxidative stress to cancer-induced cachexia in the presence or in the absence of moderate exercise training. Mice bearing the colon C26 carcinoma, either sedentary or exercised, were used. The former showed muscle wasting and redox imbalance, with the activation of an antioxidant response and with upregulation of markers of proteasome-dependent protein degradation and autophagy. Moderate exercise was able to relieve muscle wasting and prevented the loss of muscle strength; such a pattern was associated with reduced levels of Reactive Oxygen Species (ROS), carbonylated proteins and markers of autophagy and with improved antioxidant capacity. The muscle of sedentary tumor hosts also showed increased levels of molecular markers of mitophagy and reduced mitochondrial mass. Conversely, exercise in the C26 hosts led to increased mitochondrial mass. In conclusion, moderate exercise could be an effective non-pharmacological approach to prevent muscle wasting in cancer patients, decreasing muscle protein catabolism and oxidative stress and preserving mitochondria.