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Aim: To investigate the therapeutic effect of epigallocatechin gallate (EGCG) on hyperlipidemic fatty liver and its possible mechanisms in rats.Methods: Rat model with hyperlipidemic fatty liver was successfully established by feeding fatty milk for 6 weeks. The experimental rats were then treated with EGCG 10-40 mg/kg for 6 weeks. The therapeutic and antioxidation effects of EGCG on hyperlipidemic fatty liver were observed, respectively. Histopathological changes of rat liver were observed under light and electron microscopy. Expression of adenosine monophosphate protein kinase (AMPK), peroxisome proliferator-activated receptor aleph (PPARα), cholesterol 7α-hydroxylase (CYP7A), diacylglycerol acyltransferase (DGAT) and carnitine palmitoyltransferase-I (CPT-I) mRNA in hepatic tissues was examined by real time-PCR, while expression of AMPK protein was examined by immunohistochemistry method.Results: After treatment with EGCG 10-40 mg/kg for 6 weeks, the rat serum levels of total cholesterol (TC), triglyceride (TG), low density lipoprotein-cholesterol (LDL-C), free fatty acids (FFA), alanine transaminase (ALT) and aspartate transaminase (AST) were significantly decreased as compared with the fatty liver model group(P<0.05 or P<0.01). The hepatic weight and its coefficient, the contents of TC, TG, and malondialdehyde (MDA) in hepatic tissues were also significantly decreased(P<0.05 or P<0.01), the contents of high density lipoprotein-cholesterol (HDL-C) in serum and superoxide dismutase (SOD) in hepatic tissues were obviously increased(P<0.05 or P<0.01). Importantly, the histological evaluation of rat liver demonstrated that EGCG dramatically decreased lipid accumulation(P<0.01). EGCG could significantly increase the AMPK mRNA and protein expression, PPARα, CYP7A and CPT-I mRNA expression (P<0.05 or P<0.01), decrease the DGAT mRNA expression in hepatic tissues of hyperlipidemic fatty liver rats (P<0.05 or P<0.01)Conclusion: EGCG possessed the therapeutic effect on fatty milk-induced rat fatty liver, and the mechanism might be associated with its antioxidation and regulation of the CPT-I, CYP7A and DGAT gene expression via increasing the expression of AMPK and PPARα.
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