Journal
BIOCHEMICAL PHARMACOLOGY
Volume 180, Issue -, Pages -Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.bcp.2020.114145
Keywords
20(S)-ginsenoside Rg3; Myoblast differentiation; Myotube atrophy; Akt/mTOR/FoxO3
Categories
Funding
- National Key Research and Development Program of China [2017YFC1702103, 2017YFC1702106, 2018YFC1704705]
- National Natural Science Foundation of China [U19A2013]
- Science and Technology Development Plan of Jilin Province [20190101010JH]
- Administration of Traditional Chinese Medicine of Jilin Province [2020171]
- Science and Technology Development Plan of Changchun City [18YJ013]
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We 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.
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