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Mechanistic Role of Reactive Oxygen Species and Therapeutic Potential of Antioxidants in Denervation- or Fasting-Induced Skeletal Muscle Atrophy

机译:反应性氧物种的机械作用和抗氧化剂治疗抗氧化剂的抗氧化剂诱导的骨骼肌萎缩

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摘要

Skeletal muscle atrophy occurs under various conditions, such as disuse, denervation, fasting, aging, and various diseases. Although the underlying molecular mechanisms are still not fully understood, skeletal muscle atrophy is closely associated with reactive oxygen species (ROS) overproduction. In this study, we aimed to investigate the involvement of ROS in skeletal muscle atrophy from the perspective of gene regulation, and further examine therapeutic effects of antioxidants on skeletal muscle atrophy. Microarray data showed that the gene expression of many positive regulators for ROS production were up-regulated and the gene expression of many negative regulators for ROS production were down-regulated in mouse soleus muscle atrophied by denervation (sciatic nerve injury). The ROS level was significantly increased in denervated mouse soleus muscle or fasted C2C12 myotubes that had suffered from fasting (nutrient deprivation). These two muscle samples were then treated with N-acetyl-L-cysteine (NAC, a clinically used antioxidant) or pyrroloquinoline quinone (PQQ, a naturally occurring antioxidant), respectively. As compared to non-treatment, both NAC and PQQ treatment (1) reversed the increase in the ROS level in two muscle samples; (2) attenuated the reduction in the cross-sectional area (CSA) of denervated mouse muscle or in the diameter of fasted C2C12 myotube; (3) increased the myosin heavy chain (MHC) level and decreased the muscle atrophy F-box (MAFbx) and muscle-specific RING finger-1 (MuRF-1) levels in two muscle samples. Collectively, these results suggested that an increased ROS level was, at least partly, responsible for denervation- or fasting-induced skeletal muscle atrophy, and antioxidants might resist the atrophic effect via ROS-related mechanisms.
机译:各种条件,例如废用,去神经,禁食,老化,以及各种疾病下发生的骨骼肌萎缩。虽然潜在的分子机制仍然不完全清楚,骨骼肌萎缩是密切活性氧物质(ROS)过度产生有关。在这项研究中,我们的目的是探讨ROS在骨骼肌萎缩的基因调控的角度参与,进一步探讨在骨骼肌萎缩的抗氧化剂的治疗效果。在通过去神经支配(坐骨神经损伤)萎缩小鼠比目鱼肌的微阵列数据表明,许多正调节的对ROS产生的基因表达的表达上调和许多负调节物为ROS产生的基因表达的表达下调。该ROS水平失神经支配鼠标比目鱼肌是显著增加或禁食是已经从空腹(营养缺乏)遭受C2C12肌管。这两种肌肉样品,然后用N-乙酰基-L-半胱氨酸(NAC,一个在临床上使用的抗氧化剂)或吡咯喹啉醌(PQQ,天然存在的抗氧化剂),分别进行处理。相比于非处理,既NAC和PQQ治疗(1)扭转两种肌肉样品的ROS水平的增加; (2)在衰减失神经小鼠肌肉的或在禁食C2C12肌管直径的横截面面积(CSA)的减少; (3)增加了肌球蛋白重链(MHC)水平并降低了肌肉萎缩F-盒(MAFbx)和肌肉特异性RING指-1(MuRF-1)两种肌肉样品的水平。总的来说,这些结果表明,增加的ROS水平,至少部分,负责denervation-或禁食诱导的骨骼肌萎缩和抗氧化剂可以抵御通过ROS-相关机制的萎缩效果。

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