骨骼肌
自噬
肌肉萎缩
肌萎缩
C2C12型
线粒体
细胞生物学
心肌细胞
活性氧
萎缩
内科学
化学
内分泌学
生物
细胞凋亡
生物化学
医学
肌发生
作者
Huihui Wang,Yanan Sun,Taiqi Qu,Xue-Qin Sang,Li-Mian Zhou,Yixuan Li,Fazheng Ren
标识
DOI:10.3390/ijms231911963
摘要
Age-associated loss of skeletal muscle mass and function is one of the main causes of the loss of independence and physical incapacitation in the geriatric population. This study used the D-galactose-induced C2C12 myoblast aging model to explore whether nobiletin (Nob) could delay skeletal muscle aging and determine the associated mechanism. The results showed that Nob intervention improved mitochondrial function, increased ATP production, reduced reactive oxygen species (ROS) production, inhibited inflammation, and prevented apoptosis as well as aging. In addition, Nob improved autophagy function, removed misfolded proteins and damaged organelles, cleared ROS, reduced mitochondrial damage, and improved skeletal muscle atrophy. Moreover, our results illustrated that Nob can not only enhance mitochondrial function, but can also enhance autophagy function and the protein synthesis pathway to inhibit skeletal muscle atrophy. Therefore, Nob may be a potential candidate for the prevention and treatment of age-related muscle decline.
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