Black ginseng activates Akt signaling, thereby enhancing myoblast differentiation and myotube growth

Background: Black ginseng (BG) has greatly enhanced pharmacological activities relative to white or red ginseng. However, the effect and molecular mechanism of BG on muscle growth has not yet been examined. In this study, we investigated whether BG could regulate myoblast differentiation and myotube...

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Main Authors: Soo-Yeon Lee, Ga-Yeon Go, Tuan Anh Vuong, Jee Won Kim, Sullim Lee, Ayoung Jo, Jun Min An, Su-Nam Kim, Dong-Wan Seo, Jin-Seok Kim, Yong Kee Kim, Jong-Sun Kang, Sang-Jin Lee, Gyu-Un Bae
Format: Article
Language:English
Published: Elsevier 2018-01-01
Series:Journal of Ginseng Research
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Online Access:http://www.sciencedirect.com/science/article/pii/S122684531730235X
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Summary:Background: Black ginseng (BG) has greatly enhanced pharmacological activities relative to white or red ginseng. However, the effect and molecular mechanism of BG on muscle growth has not yet been examined. In this study, we investigated whether BG could regulate myoblast differentiation and myotube hypertrophy. Methods: BG-treated C2C12 myoblasts were differentiated, followed by immunoblotting for myogenic regulators, immunostaining for a muscle marker, myosin heavy chain or immunoprecipitation analysis for myogenic transcription factors. Results: BG treatment of C2C12 cells resulted in the activation of Akt, thereby enhancing heterodimerization of MyoD and E proteins, which in turn promoted muscle-specific gene expression and myoblast differentiation. BG-treated myoblasts formed larger multinucleated myotubes with increased diameter and thickness, accompanied by enhanced Akt/mTOR/p70S6K activation. Furthermore, the BG treatment of human rhabdomyosarcoma cells restored myogenic differentiation. Conclusion: BG enhances myoblast differentiation and myotube hypertrophy by activating Akt/mTOR/p70S6k axis. Thus, our study demonstrates that BG has promising potential to treat or prevent muscle loss related to aging or other pathological conditions, such as diabetes.
ISSN:1226-8453