OBJECTIVE: To investigate the effect of Ganfukang (GFK) on connective tissue 
growth factor (CTGF) and focal adhesion kinase (FAK)/protein kinase B (PKB or 
Akt) signal pathway in a hepatic fibrosis rat model and to explore the 
underlying therapeutic molecular mechanisms of GFK.
METHODS: Fifty SD rats were randomly divided into five groups as follows: the 
control group, the model group (repeated subcutaneous injection of CCl4), and 
the three GFK treatment groups (31.25, 312.5, and 3125 mg/kg, intragastric 
administration). Reverse transcriptase-polymerase chain reaction (RT-PCR), 
Western blotting, and immunohistochemistry were used to examine the expression 
of CTGF, integrin α5, integrin β1, FAK/Akt signal pathway, cyclinD1, and 
collagen in the different-treated rats.
RESULTS: GFK attenuated the up-regulation of CTGF, integrin α5, and integrin β1 
in hepatic fibrosis rats and suppressed both the phosphorylation of FAK and the 
phosphorylation of Akt simultaneously (P<0.01). At the same time, the expression 
of cyclinD1, collagen I, and collagen III was decreased by GFK significantly 
(P<0.01).
CONCLUSIONS: CTGF and FAK/Akt signal pathway were activated in the CCl4-induced 
hepatic fibrosis rats, which contribute to increased expression of cyclinD1 and 
collagen genes. The mechanisms of the anti-fibrosis activity of GFK may be due 
to its effects against CTGF and FAk/Akt signal pathway.