Objective: To investigate the protective effects and its mechanism of Supplemental Sini San(SNS) on hepatic fibrosis in rats. Method: The immunohepatic fibrosis model was induced by intraperitoneal injection of porcine serum. Eighty Wister rats were divided into eight groups:normal control

model control

Sini San Jiawei(SNSJW) high-dose

mediate-dose and low-dose

prevention and SNS group. Except the normal control groups

all the other groups were injected with pig's serum without inactivation into abdominal cavity

twice per week and 0.5 mL each time

persisting for 10 weeks. The prevention groups were orally given with the medicines(SNSJW 7 g · kg-1

10 weeks)at the same time models wasduplicated

the other treatment groups were dealed with just as the prevention groups 6 weeks later

lasted for 4 weeks. The dose was following:SNS group 4 g · kg-1

SNSJW high-dose group 14 g · kg-1

mediate-dose group 7 g · kg-1

low-dose group 3.5 g · kg-1. The changes of hepatic fibrosis were detected. The content of liver tissue interleukin-1(IL-1) and tumor necrosis factor-alpha (TNF-α)were tested by RIA. In situ hybridization assay and immunohistochemical S-P method were used to detect the expression of transforming growth factor-β1(TGF-β1) mRNA and α-smoth muscle actin(α-SMA) mRNA and there protein in hepatic fibrosis tissues. Result: Compared with model group in SNSJW mediate-dose group

the content of HYP

IL-1

TNF-α in liver tissue was depressed significantly

the expression of TGF-β1 and α-SMA genes was significantly lower in SNSJW mediate-dose group. Conclusion: Supplemental SNS has an action on hepatic fibrosis in rats. The mechanism is related with its inhibiting the expression of TGF-β1 and α-SMA genes in rats liver.