BST204 Protects Dexamethasone-Induced Myotube Atrophy through the Upregulation of Myotube Formation and Mitochondrial Function

Ryuni Kim, Hyebeen Kim, Minju Im, Sun Kyu Park, Hae Jung Han, Subin An, Jong-Sun Kang, Sang-Jin Lee and Gyu-Un Bae
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Ryuni Kim: Research Institute of Pharmaceutical Science, College of Pharmacy, Sookmyung Women’s University, Seoul 04310, Korea
Hyebeen Kim: Molecular Cell Biology, Single Cell Network Research Center, School of Medicine, Sungkyunkwan University, Suwon 16419, Korea
Minju Im: Green Cross Wellbeing Co., Ltd., Seongnam 13595, Korea
Sun Kyu Park: Green Cross Wellbeing Co., Ltd., Seongnam 13595, Korea
Hae Jung Han: Green Cross Wellbeing Co., Ltd., Seongnam 13595, Korea
Subin An: Molecular Cell Biology, Single Cell Network Research Center, School of Medicine, Sungkyunkwan University, Suwon 16419, Korea
Jong-Sun Kang: Molecular Cell Biology, Single Cell Network Research Center, School of Medicine, Sungkyunkwan University, Suwon 16419, Korea
Sang-Jin Lee: Research Institute of Pharmaceutical Science, College of Pharmacy, Sookmyung Women’s University, Seoul 04310, Korea
Gyu-Un Bae: Research Institute of Pharmaceutical Science, College of Pharmacy, Sookmyung Women’s University, Seoul 04310, Korea

IJERPH, 2021, vol. 18, issue 5, 1-11

Abstract: BST204 is a purified ginseng dry extract that has an inhibitory effect on lipopolysaccharide-induced inflammatory responses, but its effect on muscle atrophy is yet to be investigated. In this study, C2C12 myoblasts were induced to differentiate for three days followed by the treatment of dexamethasone (DEX), a corticosteroid drug, with vehicle or BST204 for one day and subjected to immunoblotting, immunocytochemistry, qRT-PCR and biochemical analysis for mitochondrial function. BST204 alleviates the myotube atrophic effect mediated by DEX via the activation of protein kinase B/mammalian target of rapamycin (Akt/mTOR) signaling. Through this pathway, BST204 suppresses the expression of muscle-specific E3 ubiquitin ligases contributing to the enhanced myotube formation and enlarged myotube diameter in DEX-treated myotubes. In addition, BST204 treatment significantly decreases the mitochondrial reactive oxygen species production in DEX-treated myotubes. Furthermore, BST204 improves mitochondrial function by upregulating the expression of peroxisome proliferator-activated receptor-? coactivator-1? (PGC1?) in DEX-induced myotube atrophy. This study provides a mechanistic insight into the effect of BST204 on DEX-induced myotube atrophy, suggesting that BST204 has protective effects against the toxicity of a corticosteroid drug in muscle and promising potential as a nutraceutical remedy for the treatment of muscle weakness and atrophy.

Keywords: Akt/mTOR pathway; BST204; mitochondria; muscle atrophy; PGC1? (search for similar items in EconPapers)
JEL-codes: I I1 I3 Q Q5 (search for similar items in EconPapers)
Date: 2021
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