Figure 6.

17α-E2 treatment beneficially modulates fibrosis resolution genes, PPARγ and SCD1, in liver. Liver Pparγ mRNA (n = 9–12/group; A), Scd1 mRNA (n = 9–12/group; B), PPARγ protein (n = 12–17/group; C), and SCD1 protein (n = 8–14/group; D) at the conclusion of the 8-wk intervention. E: representative immunoblots of liver PPARγ, SCD1, and GAPDH at the conclusion of the 8-wk intervention. All data are shown as means ± SE and were analyzed by one-way ANOVA with Tukey’s post hoc testing. We did not indicate statistical differences between vehicle and 17α-E2 treatment groups (preventive and therapeutic), or between 17α-E2 treatment groups (preventive and therapeutic), for purposes of visual clarity. *P < 0.05, **P < 0.01, ***P < 0.005. PPARγ, peroxisome proliferator-activated receptor-γ; SCD1, stearoyl-coenzyme A desaturase 1; 17α-E2, 17α-estradiol.