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<p>The specific hepatoprotective mechanism of Fermented Panax ginseng C.A. Meyer extract (FGE) has not yet been fully elucidated. In this study, an AAPH-induced liver injury model was established to investigate the hepatoprotective effects of FGE. The hepatoprotective effects of FGE may involve the mediation of the NRF2 pathway by rare ginsenosides such as 20(R)-Rh1, 20(S)-Rg2, Rg5, 20(R)-Rg2, and 20(S)-Rh1. The results showed that FGE effectively improved pathological damage and liver dysfunction, increased SOD and GPx expression in the liver, and inhibited excessive ROS generation both in vivo and in vitro. Mechanistically, FGE regulated the mRNA and protein expression of KEAP1, HO-1, and NQO1, while enhancing NRF2 protein expression and promoting its nuclear translocation. In conclusion, the NRF2 signaling pathway activated by FGE may inhibit AAPH-induced oxidative stress and alleviate the resulting liver injury.</p> Graphical abstract <p></p>

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Fermentation of Panax ginseng C.A. Meyer extract with lactic acid bacteria exerts hepatoprotective effects via activating the NRF2 pathway

  • 期刊论文

  • 发表日期：

    2025年10月14日

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  • Jia-Jun Liang,
  • Hong-Xia Liu,
  • Jian-Gang Yan,
  • Guo Xie,
  • Wen-Li Liu,
  • Jia-Hui Lin,
  • Xiao-Min Li,
  • Xin-Liang Mao

摘要

The specific hepatoprotective mechanism of Fermented Panax ginseng C.A. Meyer extract (FGE) has not yet been fully elucidated. In this study, an AAPH-induced liver injury model was established to investigate the hepatoprotective effects of FGE. The hepatoprotective effects of FGE may involve the mediation of the NRF2 pathway by rare ginsenosides such as 20(R)-Rh1, 20(S)-Rg2, Rg5, 20(R)-Rg2, and 20(S)-Rh1. The results showed that FGE effectively improved pathological damage and liver dysfunction, increased SOD and GPx expression in the liver, and inhibited excessive ROS generation both in vivo and in vitro. Mechanistically, FGE regulated the mRNA and protein expression of KEAP1, HO-1, and NQO1, while enhancing NRF2 protein expression and promoting its nuclear translocation. In conclusion, the NRF2 signaling pathway activated by FGE may inhibit AAPH-induced oxidative stress and alleviate the resulting liver injury.

Graphical abstract