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Nobiletin Prevents D-Galactose-Induced C2C12 Cell Aging by Improving Mitochondrial Function.


ABSTRACT: 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.

SUBMITTER: Wang HH 

PROVIDER: S-EPMC9569543 | biostudies-literature | 2022 Oct

REPOSITORIES: biostudies-literature

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Nobiletin Prevents D-Galactose-Induced C2C12 Cell Aging by Improving Mitochondrial Function.

Wang Hui-Hui HH   Sun Ya-Nan YN   Qu Tai-Qi TQ   Sang Xue-Qin XQ   Zhou Li-Mian LM   Li Yi-Xuan YX   Ren Fa-Zheng FZ  

International journal of molecular sciences 20221008 19


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, inhibi  ...[more]

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