AIM: To investigate the effects of tea polythenols (TP) and epigallocatechin-3-gallate (EGCG) on alcohol-induced liver injury in rats.METHODS: Forty-eight Sprague-Dawley rats were randomly divided into normal control, model, TP treatment (100, 200 mg/kg), and EGCG treatment (50, 100 mg/kg) groups. Alco-holic liver injury was induced by ethanol plus 0.5 mL fish oil intragastically for 5 wk. Liver injury was assessed by pathological examination and serum alanine aminotransferase (ALT) levels. The plasma endotoxin and serum tumor necro-sis factor(TNF)-α, interleukin(IL)-1 and IL-18 levels were measured by enzyme linked im-munosorbent assay (ELISA). The expression of CD14, lipopolysaccharide-binding protein (LBP), TNF-α, IL-1 and IL-18 mRNA in the liver were detected by reverse transcription chain reaction (RT-PCR).RESULTS: Chronic intragastric irrigation of alcohol plus fish oil resulted in the elevated serum ALT, fatty degeneration, focal necrosis and inflammatory cell infiltration in the liver of model rats. These changes were accompanied byincreased plasma endotoxin and serum TNF-α, IL-1, IL-18 levels (P < 0.05 or P < 0.01). The ex-pression of CD14, LBP, TNF-α, IL-1, and IL-18 mRNA was also increased in the model rats. However, TP and EGCG treatment improved histological changes, and significantly decreased the levels of plasma endotoxin and serum TNF-α, IL-1, IL-18, as well as the expression of CD14, LBP, TNF-α, IL-1 and IL-18 mRNA (P < 0.05 or P < 0.01). Fatty degeneration was still observed in TP and EGCG treatment group, but focal necrosis and inflammatory cell infiltration disappeared.CONCLUSION: TP and EGCG can protect liver against necrosis and inflammation induced by alcohol, and the mechanism may involve its ef-fect on the reduction of plasma endotoxia, and inhibition of Kupffer cell activity and proinflam-matory cytokine expression and secretion.