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.
Keywords: autophagy; ginsenoside Rg2; hepatic stellate cells; hepatocytes; liver fibrosis.