3.3 PB ameliorated BDL-induced liver injury and reduced hepatic fibrosis indexes
Biliary duct ligation (BDL) in mice can cause severe hepatocyte injury and liver fibrosis, and this model has also been widely used to analyze the molecular mechanism of liver injury. H&E staining assays demonstrated that the liver histological structure of the BDL group was severely damaged. Extensive liver parenchyma necrosis and newly formed bile ducts were observed in BDL model group. As expected, these pathological changes were ameliorated by PB treatment (Figure 3A). The serum ALT, AST levels were significantly increased in the BDL mice compared with those of the sham mice, and statistical reductions in these values was observed when the BDL mice were treated with PB (Figure 3B). PB dramatically decreased liver hydroxyproline concentration caused by BDL (Figure 3C). In the BDL group, Sirius red and Masson’s trichrome stained collagen fibrils extended not only to the portal areas but also to the hepatic parenchyma. PB supplementation strongly attenuated liver collagen deposition, as shown by the substantial decrease in positively stained areas (Figure 3D). The mRNA and/or protein levels of fibrogenic markers were prominently increased in the BDL treated group compared with the control group, while they were dramatically lowered by the PB intervention (Figure 3E, F). These data indicate that PB can ameliorate the BDL-induced liver injury and may play a therapeutic role in hepatic fibrosis.