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Ginsenoside Rb1 and Rb2 upregulate Akt/mTOR signaling-mediated muscular hypertrophy and myoblast differentiation

Ga-Yeon Go1, Ayoung Jo1, Dong-Wan Seo2

  • 1Research Institute of Pharmaceutical Science, College of Pharmacy, Sookmyung Women's University, Seoul, Republic of Korea.

Journal of Ginseng Research
|May 7, 2020
PubMed
Abstract

Insights

Ginsenoside Rb1 and Rb2 promote muscle stem cell differentiation and myotube growth by activating Akt/mTOR signaling. These compounds show potential for treating age-related muscle atrophy and dystrophy.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Gerontology

Background:

  • Skeletal muscle mass and function decline with age.
  • Ginsenoside Rb1 and Rb2 activate AMP-activated protein kinase, influencing glucose homeostasis.
  • Rb1 mitigates oxidative stress in aged muscles via the PI3K/Akt/Nrf2 pathway.

Purpose of the Study:

  • To investigate the effects of ginsenoside Rb1 and Rb2 on muscle stem cell differentiation.
  • To evaluate the impact of Rb1 and Rb2 on myotube formation and growth.

Main Methods:

  • C2C12 myoblasts were treated with Rb1 and/or Rb2 to induce differentiation and myotube formation.
  • Immunoblotting and immunostaining were used to analyze myogenic marker proteins (myosin heavy chain, MyoD, myogenin).
  • Immunoprecipitation assessed MyoD/E-protein heterodimerization.

Main Results:

  • Rb1 and Rb2 enhanced myoblast differentiation and myotube hypertrophy by promoting MyoD/E-protein heterodimerization.
  • Activation of Akt/mammalian target of rapamycin (mTOR) signaling was observed.
  • Rb1 and Rb2 induced MyoD-mediated transdifferentiation of rhabdomyosarcoma cells into myoblasts, with synergistic effects on differentiation via Akt activation.

Conclusions:

  • Rb1 and Rb2 enhance myotube growth and myogenic differentiation by activating Akt/mTOR signaling.
  • These compounds induce myogenic conversion of fibroblasts.
  • Rb1 and Rb2 demonstrate potential as therapeutic agents for muscle atrophy and age-related muscular dystrophy.
Keywords:
Akt/mTOR signalingHypertrophyMyoblast differentiationRb1Rb2

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