Abstract: OBJECTIVE To investigate the role of epigallocatechin gallate(EGCG) in inhibiting de novo lipogenesis and regulating lipid metabolism in HepG2 cells through the AKT/SREBP-1/FASN signaling pathway. METHODS CCK-8 method was used to detect the cytotoxicity of EGCG at different concentrations on HepG2 cells. Oil red O staining was used to observe the effect of EGCG on steatosis of HepG2 cells induced by oleic acid and determine the content of triglyceride(TG). The mRNA levels of sterol regulatory element binding protein-1(SREBP-1) and fatty acid synthase(FASN) were detected by RT-PCR. Then protein expression levels of p-AKT^Thr308, SREBP-1 and FASN were detected by Western blotting. Moreover, the effect of EGCG on the expression levels of p-AKT^Thr308, SREBP-1 and FASN were further confirmed by transient transfection with AKT plasmid. RESULTS A large amount of lipid was accumulated in HepG2 cells induced by oleic acid, the TG content and the mRNA or protein expression levels of p-AKT^Thr308, SREBP-1 and FASN were significantly increased(P<0.05). Furthermore, the protein expression levels of p-AKT^Thr308, SREBP-1 and FASN were increased after transfection with AKT plasmid(P<0.05). After treatment with EGCG(20, 40 µmol·L^-1), intracellular lipid accumulation and TG content were significantly reduced(P<0.05), mRNA or protein expression levels of p-AKT^Thr308, SREBP-1 and FASN were decreased(P<0.05). CONCLUSION EGCG may regulate the lipid metabolism of HepG2 cells by inhibiting the de novo lipogenesis through the regulation of AKT/SREBP-1/FASN signaling pathway.