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.