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Open AccessArticle

Fermented Korean Red Ginseng Extract Enriched in Rd and Rg3 Protects against Non-Alcoholic Fatty Liver Disease through Regulation of mTORC1

1
College of Pharmacy and Medical Research Center, Chungbuk National University, Cheongju 28160, Korea
2
NOVA K-MED Co., Ltd., 1646 Yuseong-daero, HNU Innobiz Park Suite 403, Yuseong-gu, Daejeon 34054, Korea
3
College of Pharmacy, Chonnam National University, Gwangju 61186, Korea
4
Department of Pathology, School of Medicine, University of California, San Diego, CA 92093, USA
5
Biosafety Research Institute and College of Veterinary Medicine, Jeonbuk National University, Deokjin-gu, Jeonju-si 54596, Korea
*
Authors to whom correspondence should be addressed.
Nutrients 2019, 11(12), 2963; https://doi.org/10.3390/nu11122963
Received: 28 October 2019 / Revised: 28 November 2019 / Accepted: 2 December 2019 / Published: 4 December 2019
The fermentation of Korean red ginseng (RG) increases the bioavailability and efficacy of RG, which has a protective role in various diseases. However, the ginsenoside-specific molecular mechanism of the fermented RG with Cordyceps militaris (CRG) has not been elucidated in non-alcoholic fatty liver disease (NAFLD). A mouse model of NAFLD was induced by a fast-food diet (FFD) and treated with CRG (100 or 300 mg/kg) for the last 8 weeks. CRG-mediated signaling was assessed in the liver cells isolated from mice. CRG administration significantly reduced the FFD-induced steatosis, liver injury, and inflammation, indicating that CRG confers protective effects against NAFLD. Of note, an extract of CRG contains a significantly increased amount of ginsenosides (Rd and Rg3) after bioconversion compared with that of conventional RG. Moreover, in vitro treatment with Rd or Rg3 produced anti-steatotic effects in primary hepatocytes. Mechanistically, CRG protected palmitate-induced activation of mTORC1 and subsequent inhibition of mitophagy and PPARα signaling. Similar to that noted in hepatocytes, CRG exerted anti-inflammatory activity through mTORC1 inhibition-mediated M2 polarization. In conclusion, CRG inhibits lipid-mediated pathologic activation of mTORC1 in hepatocytes and macrophages, which in turn prevents NAFLD development. Thus, the administration of CRG may be an alternative for the prevention of NAFLD.
Keywords: NAFLD; fermented Korean red ginseng; mTORC1 NAFLD; fermented Korean red ginseng; mTORC1
MDPI and ACS Style

Choi, S.-Y.; Park, J.-S.; Shon, C.-H.; Lee, C.-Y.; Ryu, J.-M.; Son, D.-J.; Hwang, B.-Y.; Yoo, H.-S.; Cho, Y.-C.; Lee, J.; Kim, J.-W.; Roh, Y.-S. Fermented Korean Red Ginseng Extract Enriched in Rd and Rg3 Protects against Non-Alcoholic Fatty Liver Disease through Regulation of mTORC1. Nutrients 2019, 11, 2963.

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