Gan Shen Fu Fang ameliorates liver fibrosisin vitroandin vivoby inhibiting the inflammatory response and extracellular signal-regulated kinase phosphorylation

BACKGROUND Liver fibrosis is a common health problem worldwide and there is still a lack of effective medicines. The Chinese herbal medicine, Gan Shen Fu Fang (GSFF) is composed of salvianolic acid B and diammonium glycyrrhizinate. In this study, we observed the effects of GSFF on liver fibrosisin vivoandin vitroin an attempt to provide some hope for the treatment. AIM To observe the effects of GSFF on liver fibrosisin vivoandin vitroand investigate the mechanism from the perspective of the inflammatory response and extracellular signal-regulated kinase (ERK) phosphorylation. METHODS Common bile duct-ligated rats were used forin vivoexperiments. Hepatic stellate cells-T6 (HSC-T6) cells were used forin vitroexperiments. Hematoxylin and eosin staining and Masson staining, biochemical assays, hydroxyproline (Hyp) assays, enzyme-linked immunoasorbent assay and western blotting were performed to evaluate the degree of liver fibrosis, liver function, the inflammatory response and ERK phosphorylation. The CCK8 assay, immunofluorescence and western blotting were applied to test the effect of GSFF on HSC-T6 cell activation and determine whether GSFF had an effect on ERK phosphorylation in HSC-T6 cells. RESULTS GSFF improved liver function and inhibited liver fibrosis in common bile duct-ligated rats after 3 wk of treatment, as demonstrated by histological changes, hydroxyproline assays and collagen I concentrations. GSFF alleviated inflammatory cell infiltration and reduced the synthesis of pro-inflammatory cytokines [tumor necrosis factor-alpha (TNF-alpha) and interlukin-1 beta] and NF-kappa B. In addition, GSFF decreased ERK phosphorylation.In vitro, GSFF inhibited the viability of HSC-T6 cells with and without transforming growth factor beta 1 (TGF-beta 1) stimulation and decreased the synthesis of collagen I. GSFF had the greatest effect at a concentration of 0.5 mu mol/L. GSFF inhibited the expression of alpha-smooth muscle actin (alpha-SMA), a marker of HSC activation, in HSC-T6 cells. Consistent with thein vivoresults, GSFF also inhibited the phosphorylation of ERK and downregulated the expression of NF-kappa B. CONCLUSION GSFF inhibited liver fibrosis progressionin vivoand HSC-T6 cell activationin vitro. These effects may be related to an alleviated inflammatory response and downregulated ERK phosphorylation.