PDF(Pubmed)
Abstract：
The decline in the function and mass of skeletal muscle during aging or other pathological conditions increases the incidence of aging-related secondary diseases, ultimately contributing to a decreased lifespan and quality of life. Much effort has been made to surmise the molecular mechanisms underlying muscle atrophy and develop tools for improving muscle function. Enhancing mitochondrial function is considered critical for increasing muscle function and health. This study is aimed at evaluating the effect of an aqueous extract of Gloiopeltis tenax (GTAE) on myogenesis and muscle atrophy caused by dexamethasone (DEX). The GTAE promoted myogenic differentiation, accompanied by an increase in peroxisome proliferator-activated receptor γ coactivator α (PGC-1α) expression and mitochondrial content in myoblast cell culture. In addition, the GTAE alleviated the DEX-mediated myotube atrophy that is attributable to the Akt-mediated inhibition of the Atrogin/MuRF1 pathway. Furthermore, an in vivo study using a DEX-induced muscle atrophy mouse model demonstrated the efficacy of GTAE in protecting muscles from atrophy and enhancing mitochondrial biogenesis and function, even under conditions of atrophy. Taken together, this study suggests that the GTAE shows propitious potential as a nutraceutical for enhancing muscle function and preventing muscle wasting.
摘要：
在衰老或其他病理状况期间，骨骼肌的功能和质量下降会增加与衰老有关的继发性疾病的发生率，最终导致寿命和生活质量下降。已经做出了很多努力来推测肌肉萎缩的分子机制并开发用于改善肌肉功能的工具。增强线粒体功能被认为是增加肌肉功能和健康的关键。这项研究的目的是评估gloiopeltistenax（GTAE）的水提取物对地塞米松（DEX）引起的肌生成和肌肉萎缩的影响。GTAE促进肌源性分化，伴随着过氧化物酶体增殖物激活受体γ共激活因子α（PGC-1α）表达和成肌细胞培养中线粒体含量的增加。此外,GTAE缓解了DEX介导的肌管萎缩,该萎缩可归因于Akt介导的对Atrogin/MuRF1途径的抑制。此外，一项使用DEX诱导的肌肉萎缩小鼠模型的体内研究证明了GTAE在保护肌肉免受萎缩和增强线粒体生物发生和功能方面的功效。即使在萎缩的情况下。一起来看,这项研究表明，GTAE显示出作为增强肌肉功能和防止肌肉萎缩的营养药物的有利潜力。
