Exploration of therapeutic mechanism of CGS-ANG. A, B) Relative mRNA expression of genes related to hepatic cholesterol metabolism (A) and lipogenesis (B) in livers of mice after treatments. C) The levels of fecal cholesterol and fecal bile acid in mice after treatments. D, E) Relative mRNA expression of genes related to THR activation (D) and inflammation or fibrosis (E) in livers of mice after treatments. n = 8–10 biologically independent mice per group (n = 10 for HC and NC groups; and n = 8 for CGS 26214, CGS-ANG, and ENG groups) for A) and B). F, G) Representative immunohistochemistry images and quantitative analysis of liver F4/80 (F) and α-SMA (G). Scale bar: 100 µm. Positive areas were quantified from three randomly chosen fields per liver section from individual mice using six mice per group. n = 6 biologically independent mice per group. H) The protein levels of phospho-ERK, ERK, phospho-JNK, and JNK in the livers of different treatment groups. The band densities for phospho-ERK, ERK, phospho-JNK, and JNK were first divided by GAPDH density to correct for very small loading differences. Then, the levels of phospho-JNK/JNK and phospho-ERK/ERK were normalized to NC group. n = 8 biologically independent mice per group and every two mice were pooled as one sample. Cumulative densitometric analyses were performed from four independent gels. All data are shown as mean ± SEM. Statistical significance was calculated via one-way ANOVA with Dunnett's test for A), B), D), and E) comparing each group to NC control and ordinary one-way ANOVA with Tukey's multiple comparison test for C), F), G), and H). *P < 0.05; **P < 0.01; ***P < 0.001; and ****P < 0.0001 compared with NC control.