Objective: To set up an acute liver injury mice model by α-amanitin and evulate the hepatoprotective effect of silibinin. Method: Sixty Kunming mice were randomly divided into 6 groups and intraperitoneally injected with α-amanitin at 0.10

0.20

0.35

0.70

1.32

2.50 μg · g-1

respectively. The LD50 and LD90 of α-amanitin were calculated by the improved karber method. Another 120 Kunming mice were randomly divided into 0

12

24

36

48

60

72 h groups

the time-activity curve was established using LD50 α-amanitin. The preventive and curative effects of silibinin were investigated from mortality

prevention group using LD90 α-amanitin. The preventive experiment included different dosage of silibinin groups (10

25

50

100 μg · g-1). The curative experiment included different time point groups (10

20

40

60 min after intraperitoneal injection of α-amanitin) at silibinin of 100 μg · g-1. The death situation of mouse was observed for 7 days. Moreover

36 Kunming mice were randomly divided into the blank group

the model group

the silibininin treatment group (100 μg · g-1). The activities of aspartate aminotransferase (AST)

alanine transaminase (ALT)

and level of malonaldehyde (MDA) were detected. Pathological changes of hepatic specimens were observed. Result: The LD50 and LD90 of α-amanitin toxic peptides on acute liver injury in mice was 0.36 μg · g-1 and 0.50 μg · g-1

respectively. Preventive treament with silibinin raised the survival rate of mice. Silibin of 10 μg · g-1 could protect 70%

25 μg · g-1 could protect all animals against the action of α-amanitin 60 min before administration of LD90 α-amanitin. Curative treatment with silibinin was very effective when administered 10 min after administration of LD90 α-amanitin. The anti-α-amanitin effect diminished when silibinin was 40 min after administration of LD90 α-amanitin. Compared with the blank group

levels of AST

ALT

MDA increased

SOD activity decreased significantly in the model group (P<0.01). Compared with the model group

silibinin could significantly decrease serum ALT and AST levels

increase SOD after administration of LD50 α-amanitin. From the observation of pathological picture

it showed the structure of hepatic lobule was unclear

hepatic cell cords disordered

liver cell edema

part of vacuolar changed

spotty necrosis of liver tissue in the model group. Silibinin could improve the above pathological changes significantly. Conclusion: Silibinin has a good effect in treating the α-amanitin-induced acute liver injury.