ArticleHeliyon2023
Korean red ginseng formula attenuates non-alcoholic fatty liver disease in oleic acid-induced HepG2 cells and high-fat diet-induced rats.
Article in Heliyon, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Korean red ginseng extract ameliorates high-fat diet-induced hyperlipidemia by modulating the gut microbiota-liver metabolic axis.Journal of ginseng research · 2026Article
- Gut Microbiota-Targeted Intervention of Hyperlipidemia UsingPharmaceuticals (Basel, Switzerland) · 2025Article
- METTL3 promotes the progression of non-alcoholic fatty liver disease by mediating m6A methylation of FAS.Scientific reports · 2025Article
- Effects of Korean red ginseng on auditory, cognitive, and liver functions in a naturally aged mouse model.Journal of ginseng research · 2025Article
- Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Non-alcoholic fatty liver disease (NAFLD) is the leading chronic liver disease. We have developed a Korean Red Ginseng Formula (KRGF) containing extracts of Korean Red Ginseng (KRG), Crataegus Fructus, and Cassiae Semen. In this study, our aims were to investigate the therapeutic potential and underpinning mechanisms of KRGF in NAFLD complicated by hyperlipidemia. Methods: In the Results: KRGF exerted protective effects against NAFLD by reducing lipid accumulation and steatosis in OA-stimulated HepG2 cells and HFD-fed rats. In HFD-fed rats, KRGF effectively decreased triglyceride levels in both blood and liver tissue and modulated the expression of key regulators of lipogenesis and fatty acid oxidation. KRGF downregulated the expression of lipogenesis factors, namely C/EBPα, FAS, SREBP-1c, and PPARγ, while upregulating the expression of PPARα and CPT-1, thus promoting fatty acid oxidation. Additionally, KRGF intensified the phosphorylation of AMPK and ACC, which are two enzymes that suppress fatty acid synthesis and promote fatty acid oxidation. KRGF effectively decreased total cholesterol (TC) levels in both blood and liver tissue, and it modulated the expression of major enzymes related to TC metabolism, namely apoB, ACAT2, CYP7A1, and HMGCR. Conclusion: In conclusion, KRGF mitigated NAFLD complicated by hyperlipidemia by modulating triglyceride and cholesterol metabolism, suggesting its potential for future development in the treatment of NAFLD.
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