Figure 6

The hepatic accumulation of PPL was highly associated with cholestasis. (A) Representative images for the hepatic accumulation of PPL under different types of hepatitis mediated by the indicated triggers. Protein abundance of PPL measured by western blotting is also shown at the bottom. Equal amounts of protein from 5 mice were combined in each group for western blotting. The immunoblot for GAPDH was used as the loading control. Scale bar: 100 μm. (B) Hepatic PPL expression in vehicle- or ANIT-treated mice examined by immunohistochemical and western blotting analyses. Protein abundances of K19 and ZO-1 examined by western blotting are also shown. Four or 5 mice per group were examined. The immunoblots for GAPDH were used as the loading controls. Scale bar: 100 μm. (C) Hepatic PPL expression levels in bile duct-ligated (BDL, for indicated durations) or sham-operated mice examined by immunohistochemical and western blotting analyses. Immunoblots for K19 and ZO-1 are also shown. Five mice per group were examined. The immunoblots for GAPDH were used as the loading controls. Scale bar: 100 μm. (D) Time course of the induction of hepatic Ppl mRNA expression in wild-type mice after bile duct ligation. Five to 10 mice per group were examined. mRNA expression levels are normalized to Gapdh and are expressed as mean ± SD. The average value in the liver of untreated mice was set to 1.0. ***: P < 0.001 by one-way ANOVA with Dunnett’s test (vs. untreated). (E) Time course of the hepatic PPL accumulation in bile duct-ligated mice examined by western blotting analysis. Three mice per group were examined. The immunoblot for GAPDH was used as the loading control. (F) Representative images for the time course of the hepatic PPL accumulation in bile duct-ligated mice examined by immunohistochemical analysis. Scale bar: 100 μm.