| Objective:Establish a mouse model for the study of acute hepatic injury induced by carbon tetrachloride, galactosamine and alcohol, evulate the hepato protective effect of silibinin. Method:1. Kunming mice were randomized divided into eight groups.The mice intraperitoneal injection carbon tetrachloride(0.2%). After establishing the model about the first hour and sixth hour, the tail vein injection silibinimin on different dosages(0.1 mL/10g). And then the activity of aspartate transaminase(AST), alanine transaminase(ALT) in serum, and superoxide dismutase(SOD), malonal dehyde(MDA), reduced glutathione(GSH) in liver homogenate in every group was gauged after 24 hours. Pathological changes of liver slices were investigated as well.2. Kunming mice were randomized divided into eight groups. The mice intraperitoneal injection D-galactosamine(800 mg/kg). After establishing the model about the first hour and sixth hour, the tail vein injection silibinimin on different dosages(0.1 m L/10g). And then the activity of aspartate transaminase(AST), alanine transaminase(ALT) in serum, and superoxide dismutase(SOD), malonal dehyde(MDA), reduced glutathione(GSH) in liver homogenate in every group was gauged after 24 hours. Pathological changes of liver slices were investigated as well.3. Kunming mice were randomized divided into eight groups. The mice were given alcohol(7 mL/kg). After establishing the model about the first hour and sixth hour, the tail vein injection silibinimin on different dosages(0.1 m L/10g). And then the activity of aspartate transaminase(AST), alanine transaminase(ALT) in serum, and superoxide dismutase(SOD), malonal dehyde(MDA), reduced glutathione(GSH) in liver homogenate in every group was gauged after 24 hours. Pathological changes of liver slices were investigated as well. Result:1. The carbon tetrachloride model were compared with the normal group, the levels of AST, ALT, MDA increased, SOD and GSH decreased significantly(P < 0.01). Compared with carbon tetrachloride model, the silibinimin treatment groups(120~480 mg/kg) had decreased at the levels of AST, ALT, MDA. The levels of SOD and GSH increased(P < 0.01). Observed for pathological section, hepatic cell of the model group had lesion and inflammation, hepatic tissue of the silibinimin treatment groups had the obvious improvement.2. The D-galactosamine model were compared with the normal group, the levels of AST, ALT, MDA increased, SOD and GSH decreased significantly(P < 0.01). Compared with the galactosamine model, the silibinimin treatment groups(60~480 mg/kg) had decreased at the levels of AST, ALT, MDA. The levels of SOD and GSH increased(P < 0.01, P < 0.05). Observed for pathological section, hepatic cell of the model group had necrosis and lesion, hepatic tissue of the silibinimin treatment groups improved the symptoms.3. The alcohol model were compared with the normal group, the levels of AST, ALT, MDA increased, SOD and GSH decreased significantly(P < 0.01, P < 0.05). Compared with the alcohol model, the silibinimin treatment groups(60~480 mg/kg) had decreased at the levels of AST, ALT, MDA. The levels of SOD and GSH increased(P < 0.01, P < 0.05). Observed for pathological section, hepatic cell of the model group had necrosis and edema, hepatic tissue of the silibinimin treatment groups basically got normality. ConclusionSilibinin could well protect the acute hepatic injury by carbon tetrachlitied, D-galactosamine and alcohol caused. |