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.