Fig. 5: DSF depends on bile acid-induced hepatic FXR signaling activation to ameliorate NASH.

a Experimental design. WT and Fxr^−/− mice were randomized into 4 groups (WT, WT + DSF, Fxr^−/− and Fxr^−/−+DSF) under a CDAHFD or CDAHFD + DSF, respectively for 9 weeks. b–d Serum ALT and AST; hepatic TG. e Representative images of gross appearance of the liver histology (1 cm) and photomicrographs of fixed liver sections after staining with H&E (200 μm), ORO (200 μm), α-SMA antibody (200 μm), Masson (200 μm) and F4/80 antibody (50 μm). f Quantification of the liver index (%), NAS, fold change in ORO area, α-SMA-positive area (%), CVF (%) and F4/80-positive cells (%). a–f n = 5 individuals/group for the F4/80 IF staining; n = 10/10/6/6 individuals/group, respectively for other experiments. Each point represented an individual mouse. Differences in data were calculated by Kruskal–Wallis test or ordinary one-way ANOVA depending on the sample distribution type. Data were represented as mean ± SEM. Exact P values were all given. Data were pooled from three independent experiments. α-SMA α-smooth muscle actin, CVF collagen volume fraction, DSF disulfiram, Fxr^−/− farnesoid X receptor knockout, H&E hematoxylin and eosin, NAS NAFLD activity score, NASH nonalcoholic steatohepatitis, ORO oil red O, TG triglyceride, WT wild-type. Source data are provided as a Source Data file.