Fig. 6
Effects of oral administration of isoDCA, isoLCA and UDCA on NASH amelioration. A A mouse model of NASH was induced via a high-fat diet. After the NASH model was successfully established, UDCA, isoDCA and isoLCA were orally administered to the mice. B Concentrations of serum ALT, AST, TC and TG in the different groups. Representative C H&E, D Oil red O and (E) Sirius red-stained sections of livers from the Con, NASH, isoDCA, isoLCA and UDCA consumption groups are shown (scale bar, 50 μm). Effects of isoDCA, isoLCA and UDCA supplementation on the differentiation of F TH17 and G Treg cells in the liver. H Representative Western blots of the IL-17A, Act1, TRAF6, ERK, JNK, FOSB, IL-6, TNF-α, S100A9, IL-23R, RORγt, MMP1, PPARγ, FABP1, IL-2R and Foxp3 signatures in the livers of mice in the Con, NASH, isoDCA, isoLCA and UDCA consumption groups. I The relative expression levels of IL-17A, Act1, TRAF6, ERK, JNK, FOSB, IL-6, TNF-α, S100A9, IL-23R, RORγt, MMP1, PPARγ, FABP1, IL-2R and Foxp3 in the different groups were determined (n = 3). The data are expressed as the mean ± SEM, and one-way ANOVA was performed, followed by Tukey’s HSD test. ALT, alanine transaminase; AST, aspartate transaminase; TC, total cholesterol; TG, triglyceride; H&E, haematoxylin‒eosin staining; NIC, number of inflammatory; LDEA, lipid droplet expression area; FTEA, fibrous tissue expression area; UDCA, ursodeoxycholic acid; isoDCA, isodeoxycholic acid; isoLCA and isolithocholic acid; Con, control group; NASH, nonalcoholic steatohepatitis group; NASH-T, nonalcoholic steatohepatitis tolerance group