Effect of Thalidomide on Acute Liver Injury Induced by Carbon Tetrachloride in Mice
Objective To investigate the effect of thalidomide on the acute liver injury model mice.Methods Forty-eight C57BL/6 mice were randomly divided into the normal control group(equal volume of physiological saline),the model group(equal volume of physiological saline),the compound glycyrrhizin group(0.035 mg/g),the thalidomide low-,medium-,and high-dose groups(0.01,0.03,0.05 mg/g),with eight mice in each group.The mice were intraperitoneally injected with 0.6%carbon tetrachloride(CCl4,0.01 mL/g)to replicate the acute liver injury model,corresponding drugs or physiological saline were given by gavage at 12 h before modeling and at 12,24 h after modeling.The liver tissue mass and body mass were weighed,and the liver index was calculated.The pathological change in liver tissue of mice was observed by the hematoxylin-eosin(HE)staining.The alanine aminotransferase(ALT)and aspartate aminotransferase(AST)levels in mouse serum were detected;the expression level of tumor necrosis factor-α(TNF-α)in liver tissue homogenates of mice was detected by the enzyme-linked immunosorbent assay;the expression level of CD68 protein in liver tissue homogenates of mice was detected by the Western blot.Results Compared with those in the model group,the liver cell necrosis and inflammatory infiltration in the compound glycyrrhizin group and thalidomide medium-dose group relieved;the liver index and serum ALT and AST levels in the compound glycyrrhizin group and thalidomide low-,medium-,and high-dose groups significantly decreased(P<0.05);the expression level of TNF-α in the liver tissue homogenates in the compound glycyrrhizin group and thalidomide medium-,and high-dose groups significantly decreased(P<0.01);the expression level of CD68 protein in the liver tissue homogenates in the compound glycyrrhizin group and thalidomide medium-dose group significantly decreased(P<0.05).Conclusion Thalidomide can significantly improve the CCl4-induced acute liver injury in mice,and its mechanism may be related to the inhibition of transaminase activity and CD68 protein expression.