Abstract: The effects of quercetin-3-O-β-D-glucuronide(Q3GA)on the triglyceride metabolism and oxidative stress in steatotic HepG2 cells and the underlying mechanism were investigated in this study. Significant fat accumulation was documented by Oil Red O staining; intracellular triglyceride levels were detected by triglyceride(TG)enzymatic assay. DCFH-DA staining assay was performed to observe reactive oxygen species(ROS)production of HepG2 cells. The level of malondialdehyde(MDA)and superoxide dismutase(SOD)were assayed by thibabituric acid method and xanthine oxidase method. Changes in the mRNA expression of peroxisome proliferator-activated receptor α(PPARα), carnitine palmitoyltransferase 1A(CPT1A), medium chain acyl-CoA dehydrogenase(MCAD), cytochrome P450 4A11(CYP4A11)and acyl-CoA oxidase(ACO), which are related with fatty acid oxidation were assessed by RT-PCR. Our results showed that Q3GA obviously reduced fat deposition and TG content. At the same time, Q3GA decreased MDA content and significantly increased the SOD activity with reduced ROS production. Moreover, the PPARα, CPT1A, MCAD expression-related fatty acid β oxidation was upregulated with the treament of Q3GA, while without any change of the expression of CYP4A11, ACO. In conclusion, Q3GA prevents FFA-induced HepG2 cell steatosis, and enhances mitochondrial fatty acid β oxidation, which may partly be related to its anti-oxidation ability.