Objective:To observe the effect of Langqing Ata (LQAT) on the metabolism of collagen in rat hepatic fibrosis model. Method: Composite factors (subcutaneous injection of 40% CCl4/olive oil solution+high-fat and low-protein compound feed+give 5% ethanol drinking water) were used to establish rat liver fibrosis model. Except the normal control group

the model rats were divided into five groups as model group

Fufang Biejia Ruangan table group(0.55 g·kg-1) and LQAT groups at three doses(11.4

5.7

2.85 g·kg-1 respectively). The rats were orally treated with corresponding decoctions once a day for 7 weeks. At the end of the dosing cycle

rats were sacrificed and livers were collected and then were dyed by hematoxylin-eosin staining to observe the pathological changes. The degree of fibrosis in liver tissue was observed by Masson staining. The expression levels of tissue inhibitor of metal protease 1(TIMP-I) in liver tissue were detected by immunohistochemistry method. The expression levels of type 1 collagen(CoL-I) mRNA in livers were measured by Real-time fluorescence quantitative PCR (RTFQ PCR). Result: The fiber tissue proliferation and liver inflammation activity on the hepatic fibrosis could be ameliorated by the high and middle dose groups (P<0.05-P<0.01). The immunohistochemical results showed that LQAT significantly reduced the expression levels of TIMP-I in livers (P<0.01). Results also showed the dose-dependent inhibition of LQAT on the expression levels of CoL-I mRNA in livers

and the high dose group showed significant difference (P<0.01) compared with the model group. Conclusion: LQAT played the role of anti-liver fibrosis by significantly improving hepatic fibrous tissue proliferation

and reducing the expression of TIMP-I and CoL-I mRNA.