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

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 ag...

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Bibliographic Details
Published in:International journal of molecular sciences 2022-10, Vol.23 (19), p.11963
Main Authors: Wang, Hui-Hui, Sun, Ya-Nan, Qu, Tai-Qi, Sang, Xue-Qin, Zhou, Li-Mian, Li, Yi-Xuan, Ren, Fa-Zheng
Format: Article
Language:English
Subjects:
Aging
Aging (artificial)
Antioxidants
Apoptosis
Atrophy
Autophagy
C2C12 myoblast
Cell cycle
D-Galactose
Galactose
Homeostasis
Inflammation
Kinases
Metabolism
Mitochondria
mitochondrial function
Muscles
Musculoskeletal system
Myoblasts
nobiletin
Older people
Organelles
Oxidative stress
Population studies
Prevention
Protein biosynthesis
Protein folding
Protein synthesis
Proteins
Reactive oxygen species
Respiration
ROS
Senescence
Skeletal muscle
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Summary: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.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms231911963