Ginsenoside Rg2 Ameliorating CDAHFD-Induced Hepatic Fibrosis by Regulating AKT/mTOR-Mediated Autophagy
Ziwei He, Siyu Chen, Tingting Pan, Ao Li, Kangyu Wang, Zhuofeng Lin, Wei Liu, Yi Wang, Yanfang Wang
Abstract
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.