Objective To explore the possible mechanism of Biejiajian Pill（ 鳖甲煎丸

BJJP） in the treatment of hepatic fibrosis. Methods Forty-eight rats were randomly divided into blank control group

model group

colchicine group

and BJJP low

medium

and high dose groups

with 8 rats in each group. Except the blank control group

rats in the other groups were injected intraperitoneally with carbon tetrachloride（ CCl4） to establish a hepatic fibrosis model. On the 2 nd day after the first injection

the low

medium

and high doses of BJJP were administered to BJJP 0. 55

1. 1

and 2. 2 g/（ kg·d） gavage

respectively. The colchicine group was given Colchicine tablets suspension 0. 11 mg/（ kg·d） gavage. Blank control group and model group were given 2 ml saline gavage

for a total of8 weeks. Masson staining was used to observe the pathological changes of liver. Serum alanine aminotransferase（ ALT）

aspartate aminotransferase（ AST）

liver function index and superoxide dismutase（ SOD）

malondialdehyde（ MDA）

hydroxyproline（ HYP）

transforming growth factor beta 1（ TGF-β1）

connective tissue growth factor（ CTGF）

tumor necrosis factor α（ TNF-α）

and vascular endothelial growth factor（ VEGF） level were detected.Western blot was used to detect the expression of β-catenin

glycogen synthase kinase 3β（ GSK-3β）

phosphorylated glycogen synthase kinase 3β（ p-GSK-3β）

protein kinase B（ AKT） and phosphorylated protein kinase B（ p-AKT）.Results Compared with the model group

the fibrous tissue hyperplasia was significantly reduced in different doses of BJJP groups. Serum ALT

AST levels and levels of MDA

HYP

TGF-β1

CTGF

TNF-α and VEGF were decreased and SOD levels were increased（ P < 0. 05）. The expression of β-catenin

p-GSK-3β and p-AKT protein in liver tissue was significantly reduced

and the effect of high dose of BJJP was better（ P < 0. 05）. There was no significant difference in the expression of GSK-3β and AKT protein of the liver tissues in each group（ P > 0. 05）. Conclusion BJJP can significantly reduce the degree of hepatic fibrosis induced by CCl4 in rats

which may be related to its inhibition of the activation of Wnt/β-catenin signaling pathway and the decrease of its downstream target gene expression.