To study the hypolipidemic effect of complanatoside A on steatosis L02 cells and the mechanism.Methods:Free fatty acid(FFA) was used to induce steatosis in human liver L02 cells.The cells were classified into the blank group，model group，and low-dose，medium-dose，and high-dose complanatoside A groups(1 μmol/L，10 μmol/L，and 50 μmol/L，respectively).Apoptosis and fat accumulation were detected by flow cytometry.The levels of triglyceride(TG)，total cholesterol(TC)，malondialdehyde(MDA)，and superoxide dismutase(SOD) were determined with corresponding kits.The mRNA expression of adipose triglyceride lipase(ATGL)，peroxisome proliferator-activated receptor(PPAR)-α，PPAR-γ，tumor necrosis factor(TNF)-α，and interleukin-6(IL-6) was measured by qPCR，and the protein expression of ATGL，PPAR-α，PPARγ，TNF-α，and IL-6 by Western Blotting.Results:Complanatoside A reduced fat accumulation，content of TG，TC，and MDA，and apoptosis rate，enhanced SOD activity，and alleviated liver cell injury caused by lipotoxicity as compared with the model group(P<0.05，P<0.01).Complanatoside A raised the mRNA and protein expression of ATGL，PPAR-α，and PPARγ and lowered the mRNA and protein expression of TNF-α and IL-6 in comparison with the model group(P<0.01).Conclusion:Perhaps by up-regulating the expression of PPAR-α and PPAR-γ，complanatoside A can increase the expression of ATGL，promote the hydrolysis of liver TG，reduce the deposition of fat in liver，alleviate oxidative stress，inhibit the secretion of TNF-α and IL-6，and relieve inflammation，so as to restore the normal function of hepatocytes.