Fig. 5. Fas/FasL repressed the activation of NF-κBp65 in hepatocytes in liver fibrogenesis.

a Immunohistochemical staining (brown) of Fas, FasL, and p-p65 (the phosphorylation of NF-κBp65) in the indicated liver sections was presented (n = 6 per group). b Expressions of Fas, FasL, p65, p-p65, and COL-I proteins from the related humans liver sections were detected by western blotting. c Western blotting was adopted to analyze the levels of Fas, FasL, p65, p-p65, and COL-I in the liver tissues of mouse models. The ratio of densitometry units of the normalized Fas/β-actin and p-p65/β-actin from (b) and (c) was also determined, n = 6 per group, values are presented as mean ± SEM. *P < 0.05. CTRL, the control mice (olive oil-treated mice); CCl₄, 20% carbon tetrachloride-induced mouse fibrosis; Normal, healthy volunteers; LF, human liver fibrosis. d Western blotting depicted that knockdown of Fas upregulated the level of p-p65 in the primary hepatocytes isolated from CCl₄-treated mice. The ratio of densitometry units of the normalized p65/β-actin and p-p65/β-actin was also presented, n = 6 per group, values are presented as mean ± SEM. *P < 0.05 versus primary hepatocytes from CTRL group, ^#P < 0.05 versus primary hepatocytes from CCl₄-treated group without siFas treatment. e FasL treatment enhanced the expression of Fas and repressed the phosphorylation of NF-κBp65 (p-p65) in the primary hepatocytes, while knockdown of Fas by siRNA upregulated the level of p-p65 in FasL-treated group. The ratio of densitometry units of the normalized p65/β-actin and p-p65/β-actin was also presented, n = 6 per group, values are presented as mean ± SEM. *P < 0.05 versus primary hepatocytes from PBS group, ^#P < 0.05 versus primary hepatocytes from FasL-treated group without siFas treatment.