Figure 2. CDDO-Me improves NASH in CDAHFD-fed mice
(a) Experimental design for CDDO-Me treatment of CDAHFD-fed mice (n = 8). (b) Representative images of HE-stained liver sections. Scale bars show 100 μm (upper panels) and 20 μm (lower panels). (c) The scores for steatosis, lobular inflammation, hepatocyte ballooning, and NAS. Statistical differences were analysed using a non-parametric Kruskal-Wallis test followed by a Dunn-Bonferroni post-hoc test (*P < 0.05; **P < 0.01; ***P < 0.001, ****P < 0.0001, versus vehicle-treated CDAHFD-fed mice, mean + S.D., n = 8). (d-g) mRNA expression of Tnfa (d), Ifng (e),Abcg5 (f), and Ces2c (g) determined using quantitative PCR (mean + S.D., n = 8). Statistical differences were analysed using Dunnett’s multiple comparison test (*P < 0.05; **P < 0.01; ***P < 0.001, ****P < 0.0001, versus vehicle-treated CDAHFD-fed mice). Cont, Control; Veh, Vehicle. ns; not significant.
Figure 3. CDDO-Me reduces oxidative stress in the liver of CDAHFD-fed mice
(a) Hepatic MDA levels measured in the liver homogenates of CDAHFD-fed mice treated without or with the indicated concentrations of CDDO-Me (mean + S.D., n = 8). (b and c) mRNA expression of Nqo1 (b) andGclc (c) determined using quantitative PCR (mean + S.D., n = 8). Statistical differences were analysed using Dunnett’s multiple comparison test (*P < 0.05; **P < 0.01; ***P < 0.001, ****P < 0.0001 versus vehicle-treated CDAHFD-fed mice). (d) NQO1, GCLC, and Vinculin protein levels determined by immunoblotting. (e and f) Densitometric analyses of Figure. 3d were normalized to Vinculin levels (mean + S.D., triplicate). Cont, Control; Veh, Vehicle. ns; not significant.