Objective: The aim of our study is to investigate the effect of Yulangsan flavonoids(YLSF) against CCl4-induced liver fibrosis in rats and study its mechanism. Method: The SD rats were divided into two groups randomly: hepatic fibrosis group and normal control group (NC). The rats of hepatic fibrosis group were induced by intragastric administration (ig) of 50% CCl4

and rats in NC group were given normal saline (NS). The rats of hepatic fibrosis group confirmed by the pathological inspection were divided into 2 groups randomly:Drug intervention group and the model group which were treated with NS. The drug intervention group was divided randomly into 3 different does YLSF groups (20

40

80 mg · kg-1) and a positive control group (colchicine tablets 0.20 mg · kg-1). All rats were treated with drugs or NS for four consecutive weeks ig

one time a day. Twenty-four hours after the last administration of drugs

all rats were sacrificed

and the blood serum and hepatic tissue were taken quickly. The activities of alanine transaminase(ALT) and aspartale transaminase (AST) in the serum and the levels of superoxide dismutase(SOD)

malonaldehyde(MDA)

glutathione(GSH)

and glutathione synthesis (GSH-Px) in hepatic tissue were analyzed

and the degree of hepatic injury was examined. Result: The content of AST

ALT in serum of each YLSF groups’ rats were (207.85±101.72)

(131.55±35.09)

(129.98±37.21) U · L-1

(90.51±44.24)

(47.79±16.11)

(44.56±16.31) U · L-1;and the content of SOD

MDA

GSH-Px

GSH in the tissue of each YLSF groups’ rats were (143.14±42.82)

(146.53±31.98)

(147.41±32.82) U · mg-1

(2.57±0.54)

(2.19±0.57)

(2.11±0.59) nmol · mg-1

(463.55±271.07)

(659.14±162.23)

(752.08±200.70) nmol · mg-1

(5.06±1.09)

(6.10±0.97)

(6.89±0.98) nmol · mg-1. Compared with the model control group

the increased activity of AST in serum and the increased content of MDA in liver induced by CCl4 were decreased significantly

and the decreased levels of SOD in liver was increased significantly in all dose of YLSF groups and positive control group. The activity of ALT in serum was decreased significantly (P<0.01) and the content of GSH (P<0.01) in liver was increased in the high dose and the middle dose of YLSF groups and positive control group. Meanwhile the activity of GSH-Px in the liver was increased significantly in the high dose and the middle dose of YLSF groups (P<0.01). The degree of hepatic injury in all dose of YLSF groups and positive control group could be lessened (P<0.05 or P<0.01). Conclusion: Our findings demonstrate that YLSF has a certain curative effect on CCl4-induced liver fibrosis in rats

and its mechanism maybe involve in attenuating free radical and inhibiting the lipid peroxidation.