FIGURE 2.

CKI ameliorates inflammatory response, oxidative stress, cell compensatory proliferation, and hepatocellular death in the mice liver. (A) Mice were intraperitoneally treated with 4 ml/kg CCl₄ for 6 weeks along with CKI treatment (7.5 ml/kg) for 3 weeks. The proportion of macrophages in mice liver tissues was detected by flow cytometry after indicated treatments (right). Representative flow cytometry gating images are shown (left). (B) Representative F4/80 immunostaining of macrophages in mice liver sections were displayed (original magnification 20 × 10, scale bar 100 μm). (C) Serum levels of TNFα and IL‐6 were detected by Elisa assays in CCl₄‐induced (n = 9) or MCD diet‐induced (n = 8) liver fibrosis models. (D) Serum levels of superoxide dismutase (SOD) and malondialdehyde (MDA) were quantified by Elisa assays in CCl₄‐challenged (n = 10) or MCD diet‐challenged (n = 8) mice. (E) Representative immunostaining of PCNA in the liver section of mice are shown after indicated treatments (original magnification 20 × 10, scale bar 100 μm). (F) Representative immunostaining of cleaved caspase 3 in the mice liver tissues are shown after indicated treatments (original magnification 10 × 10, scale bar 210 μm). (G) Expression of cytochrome C, cleaved caspase 3, and cleaved PARP in liver tissue lysates were determined by Western blot from CCl₄‐challenged (above) or MCD diet‐challenged (below) mice. Data are presented as means ± SEM. ns, p > 0.05; *p < 0.05; **p < 0.01; ***p < 0.001