Oleanolic acid alleviates obesity-induced skeletal muscle atrophy via the PI3K/Akt signaling pathway.
Yaqin Sun, Xiaofang Wei, Tong Zhao, Hongwei Shi, Xiaojing Hao, Yue Wang, Huiling Zhang, Zhichao Yao, Minxing Zheng, Tianyun Ma, Tingting Fu, Jiayin Lu, Xiaomao Luo, Yi Yan, Haidong Wang
Author Information
Yaqin Sun: College of Veterinary Medicine, Shanxi Agricultural University, Jinzhong, China.
Xiaofang Wei: College of Veterinary Medicine, Shanxi Agricultural University, Jinzhong, China.
Tong Zhao: College of Veterinary Medicine, Shanxi Agricultural University, Jinzhong, China.
Hongwei Shi: College of Veterinary Medicine, Shanxi Agricultural University, Jinzhong, China.
Xiaojing Hao: College of Veterinary Medicine, Shanxi Agricultural University, Jinzhong, China.
Yue Wang: College of Veterinary Medicine, Shanxi Agricultural University, Jinzhong, China.
Huiling Zhang: College of Veterinary Medicine, Shanxi Agricultural University, Jinzhong, China.
Zhichao Yao: College of Veterinary Medicine, Shanxi Agricultural University, Jinzhong, China.
Minxing Zheng: College of Veterinary Medicine, Shanxi Agricultural University, Jinzhong, China.
Tianyun Ma: College of Veterinary Medicine, Shanxi Agricultural University, Jinzhong, China.
Tingting Fu: College of Veterinary Medicine, Shanxi Agricultural University, Jinzhong, China.
Jiayin Lu: College of Veterinary Medicine, Shanxi Agricultural University, Jinzhong, China.
Xiaomao Luo: College of Veterinary Medicine, Shanxi Agricultural University, Jinzhong, China.
Yi Yan: College of Veterinary Medicine, Shanxi Agricultural University, Jinzhong, China.
Haidong Wang: College of Veterinary Medicine, Shanxi Agricultural University, Jinzhong, China. ORCID
中文译文
English
Oleanolic acid (OA) is a pentacyclic triterpene with reported protective effects against various diseases, including diabetes, hepatitis, and different cancers. However, the effects of OA on obesity-induced muscle atrophy remain largely unknown. This study investigated the effects of OA on skeletal muscle production and proliferation of C2C12 cells. We report that OA significantly increased skeletal muscle mass and improved glucose intolerance and insulin resistance. OA inhibited dexamethasone (Dex)-induced muscle atrophy in C2C12 myoblasts by regulating the PI3K/Akt signaling pathway. In addition, it also inhibited expression of MuRF1 and Atrogin1 genes in skeletal muscle of obese mice suffering from muscle atrophy, and increased the activation of PI3K and Akt, thereby promoting protein synthesis, and eventually alleviating muscle atrophy. Taken together, these findings suggest OA may have potential for the prevention and treatment of muscle atrophy.
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20210302124700/The Young Science Foundation of Shanxi province
202103021223166/The Young Science Foundation of Shanxi province
20211331-16/Shanxi "1331 Project" Key Innovative Research Team
20211331-13/Shanxi "1331 Project" Key Innovative Research Team
2021L132/Shanxi Province Colleges and Universities Science and Technology Innovation Project
SXBYKY2021043/The Excellent Doctoral Work Award-Scientific Research Project of Shanxi Province
SXBYKY2022039/The Excellent Doctoral Work Award-Scientific Research Project of Shanxi Province
32102634/The National Natural Science Foundation of China
2021BQ08/Start-up Fund for doctoral research, Shanxi Agricultural University
2021BQ69/Start-up Fund for doctoral research, Shanxi Agricultural University
Animals
Mice
Muscle, Skeletal
Muscular Atrophy
Obesity
Oleanolic Acid
Phosphatidylinositol 3-Kinases
Proto-Oncogene Proteins c-akt
Signal Transduction
Oleanolic Acid
Phosphatidylinositol 3-Kinases
Proto-Oncogene Proteins c-akt