氧化应激在衰老性肌萎缩中的作用机理与运动干预探讨

Etiological role of oxidative stress in sarcopenia and exercise intervention

与衰老相关的骨骼肌质量、力量下降称为衰老性肌萎缩。衰老时骨骼肌内氧化应激增强会导致线粒体机能下降、分子炎症,这些因素相互作用诱导肌纤维凋亡,并干扰蛋白质代谢平衡,这可能是衰老性肌萎缩的重要机制。遗传操作研究和运动锻炼研究已证明转录辅激活因子PGC-1α表达增强有利于降低ROS生成并增强线粒体生物合成,降低炎症基因转录。激活蛋白激酶Akt可促进肌肉蛋白质合成,还可抑制蛋白质分解和凋亡。通过运动训练调节PGC-1α、Akt的表达和活性可能是运动干预部分地逆转衰老性肌萎缩的内在机制。探讨衰老性肌萎缩的细胞分子机制及运动干预的作用,在此基础上提出未来研究的方向。

Aging is closely associated with the reduction of skeletal mass and strength and is termed as sarcopenia of aging. With the increasing of age, oxidative stress leads to mitochondrial dysfunction and chronic molecular inflammation, and the interaction of which may induce apotosis of muscle fi- bers, and intervene the balance of protein synthesis. Using genetically manipulated models and undergoing exercise has demonstrated that PGC--Ia has a powerful suppressive effect on ROS production, in parallell with its effects in elevating mitochondrial respiration and the down regulation of expression of pro--inflammatory genes. Aetiviation of Akt leads to glucose uptake, glycogen synthesis, and protein synthesis, and also inhibits apoptosis and protein degradation. Exercise may partly reverse sarcopenia of aging via modulation of the expression and activity of transcription coactivator PGC-1α and protein kinase Akt. The main is to investigate the molecular and cellular mechanisms underlying sarcopenia and the effect of exercise intervention, by which the future directions will be pointed out.