Ginsenoside Rg2 Ameliorating CDAHFD-Induced Hepatic Fibrosis by Regulating AKT/mTOR-Mediated Autophagy
- J Agric Food Chem. 2022 Feb 16;70(6):1911-1922. doi: 10.1021/acs.jafc.1c07578.
- 1. College of Chinese Medicinal Materials, Jilin Agricultural University, Changchun 130118, China.
- 2. School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou 325035, China.
- 3. College of Life Science, Jilin Agricultural University, Changchun 130118,China.
- 4. College of Foreign Languages, Jilin Agricultural University, Changchun 130118, China.
- 5. Research Center Ginseng Genetic Resources Development and Utilization, Changchun 130118, China.
- 6. Laboratory for Cultivation and Breeding of Medicinal Plants of National Administrition of Traditional Chinese Medicine, Changchun 130118, China.
Ginsenoside Rg2 (G-Rg2) in the rhizome of Panax ginseng can modify lipid accumulation, oxidative stress, and Apoptosis in the liver induced by a high-fat diet. This research adds to this by assessing the potential antifibrosis effect of G-Rg2 (including possible mechanisms). G-Rg2 significantly improved pathological changes in liver tissue induced by a choline-deficient, l-amino acid-defined, high-fat diet (CDAHFD), it inhibited serum transaminase, plasma lipopolysaccharide, and liver hydroxyproline levels; it inhibited TGF-β1, α-SMA, and COL1A1 expression, it activated the Akt/mTOR signal pathway, and it inhibited liver expression of autophagy-related proteins. The in vitro experiments showed that G-Rg2 also restored the Autophagy flux impairment induced by oleic acid and inhibited TGF-β1 expression by promoting p62 degradation in hepatocytes. In hepatic stellate (HSC-T6) cells, G-Rg2 reversed lipopolysaccharide-induced activation through the Akt/mTOR signaling pathway, inhibiting Autophagy. Thus, G-Rg2 ameliorates CDAHFD-induced liver fibrosis and lipopolysaccharide-induced HSC-T6 cell activation by inhibiting Akt/mTOR-mediated Autophagy.
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Cat. No.Product NameDescriptionTargetResearch Area
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target: mTOR; FKBP; Molecular Glues; Fungal; Autophagy; Endogenous Metabolite; Antibiotic; Bacterial
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