Objective:To study the effects of epigallocatechin-3-gallate(EGCG)on transferrin(Tf)in liver of mice with alcoholic liver disease(ALD) and to explore its mechanisms. Method: C57/BL6 mice were randomly divided into two groups: normal group and model group. Alcoholic liver disease was induced by gavage of alcohol for 12 weeks. At the end of 8 weeks

the alcohol group was divided into four subgroups: model group

EGCG (20 mg·kg-1) group

EGCG (10 mg·kg-1) group

EGCG (30 mg·kg-1) group. Mice in the EGCG groups were received an intraperitoneal injection of EGCG via simultaneous intragastric administration with normal saline or alcohol for 4 weeks. Liver injuries were assessed by histopathologic examination and serum alanine aminotransferase(ALT)

aspartate aminotransferase(AST)levels. In addition

liver iron levels and Tf

transferin receptor 1(TfR1)of liver tissue were evaluated. Result: Model group mice had marked increase in serum ALT

AST levels and liver iron concentration compared with normal group

and their liver tissues showed moderate hepatocytes fatty degeneration. However

every treatments groups resulted in decreased ALT

AST levels and liver iron concentration and improved pathological changes. Liver Tf and TfR1 protein expression levels were elevated significantly in model group compared with normal group

but markedly suppressed by EGCG treatments. Conclusion: Compared with model group

treatment of ALD mice with EGCG decreased Tf and TfR1 protein expression in the liver. EGCG might play a protective role in the development of ALD. This beneficial effect of EGCG may be attributed to its iron chelation ability. The possible mechanisms is that EGCG decreases the hepatic iron uptake by the downregulation of Tf and TfR1.