Suppressive effects of 17β-estradiol on hepatic fibrosis in CCl4-induced rat model

Figure 1 Histopathological findings of representative liver sections from female rats treated with CCl_4. VG staining, original magnification ×100. A: Control group; B: Ovx+CCl₄ group; C: Ovx + CCl₄ + β-Est group.

Figure 2 Immunohistochemistry of α-SMA in representative liver sections from female rats treated with CCl₄, DAB staining. A: control group, original magnification ×200; B: Ovx + CCl₄ group, original magnification × 400; C: Ovx + CCl₄ + β-Est group, original magnification ×400.

Figure 3 Histopathological and immunohistochemical changes in CCl₄-treated female rats (fibrotic area percentage of total field), ^aP<0. 05 vs CCl₄; ^bP<0.01 vs control.

Figure 4 Serum estradiol levels in CCl₄–treated female rats, ^bP<0. 01 vs control, ^dP<0.01 vs CCl₄.

Figure 5 Negative correlation between fibrotic area percentage and serum estradiol level (r = 0. 57, P < 0.01).

Figure 6 Effects of estradiol metabolites on function of HSCs proliferation (A), HA (B) and C IV (C) secretion in HSCs, effects of 10^-7 mol/L estradiol metabolites on α-SMA expression (D) of HSCs. Values for each point represent mean ± SD from 5 separate experiments, ^aP < 0.05 vs control, ^dP < 0.05 vs 10^-7 mol/L β-Est.

Figure 7 Representative immunohistochemistry showing expression of ER on HSCs used for studies, original magnification ×200. No expression of ER-α(A) but ER-β(B) was observed.