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Biochemical pharmacology · Oct 2020
20(S)-ginsenoside Rg3 promotes myoblast differentiation and protects against myotube atrophy via regulation of the Akt/mTOR/FoxO3 pathway.
- Manying Wang, Jixiang Ren, Xuenan Chen, Jianzeng Liu, Xiaohao Xu, Xiangyan Li, Daqing Zhao, and Liwei Sun.
- Research Center of Traditional Chinese Medicine, the Affiliated Hospital to Changchun University of Chinese Medicine, 1478 Gongnong Street, Changchun, Jilin Province 130021, PR China; Jilin Ginseng Academy, Changchun University of Chinese Medicine, 1035 Boshuo Road, Changchun, Jilin Province 130021, PR China.
- Biochem. Pharmacol. 2020 Oct 1; 180: 114145.
AbstractWe previously found that 20(S)-ginsenoside Rg3 (S-Rg3) promotes myoblast differentiation via an unknown mechanism. Here we measured levels of myosin heavy chain (MHC) and myogenin, markers of myoblast differentiation, using Western blot analysis and immunofluorescence staining. Notably, S-Rg3 treatment of C2C12 myoblasts led to increased muscle differentiation and protection from muscle atrophy in a dexamethasone (DEX)-treated C2C12 myotube-based muscle atrophy model. This effect was likely caused by S-Rg3 treatment-induced promotion of Akt/mTOR phosphorylation and inhibition of FoxO3 nuclear transcription. Additionally, S-Rg3 treatment also led to increased fruit fly climbing distances (Drosophila melanogaster) and prevented muscle atrophy in aged fruit flies. Our study provides a mechanistic framework for understanding how S-Rg3 enhances myoblast differentiation and inhibits myotube atrophy through activation of the Akt/mTOR/FoxO3 signaling pathway, as demonstrated in vitro in C2C12 cells and in vivo in fruit flies.Copyright © 2020 Elsevier Inc. All rights reserved.
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