ArticleInternational journal of environmental research and public health2021
BST204 Protects Dexamethasone-Induced Myotube Atrophy through the Upregulation of Myotube Formation and Mitochondrial Function.
Article in International journal of environmental research and public health, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.
- A Systematic Review and User Reference of Phenotypic and Molecular Characteristics of Dexamethasone-Mediated C2C12 Muscle Atrophy.Journal of cachexia, sarcopenia and muscle · 2026Pooled it
- The Effect of Dexamethasone-Mediated Atrophy on Mitochondrial Function and BCAA Metabolism During Insulin Resistance in C2C12 Myotubes.Metabolites · 2025Article
- Hyperphosphatemia Contributes to Skeletal Muscle Atrophy in Mice.International journal of molecular sciences · 2024Article
- Potential of Lycii Radicis Cortex as an Ameliorative Agent for Skeletal Muscle Atrophy.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Effects of the purified dry extract of fermented ginseng BST204 on muscle fiber regeneration.Biochemistry and biophysics reports · 2023Article
- A Comprehensive Review of Pathological Mechanisms and Natural Dietary Ingredients for the Management and Prevention of Sarcopenia.Nutrients · 2023Review
- Hypoglycemic drug liraglutide alleviates low muscle mass by inhibiting the expression of MuRF1 and MAFbx in diabetic muscle atrophy.Journal of the Chinese Medical Association : JCMA · 2023Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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-γ coactivator-1α (PGC1α) 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.
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