AimTo investigate the effects of peroxisome proliferator-activated receptor-γ(PPARγ) on cholesterol accumulation and CD36 expression in THP-1 macrophages.MethodsMononuclear cells were induced to differentiate into THP-1 macrophages by phorbol myristate acetate (160 nmol/L) co-incubation for 24 h.THP-1 macrophages were co-incubated with 50 mg/L oxidize low-density lipoprotein (ox-LDL) and PPARγ agonist Ciglitazone（10 μmol/L;C）and PPARγ antagonist GW9662（10 μmol/L;D）for 24 h, and the cells mixed with (B) and without (A) ox-LDL were as the control groups.Cellular total cholesterol was determined by high performance liquid chromatography analysis.CD36 mRNA and protein levels were determined by reverse transcription-polymerase chain reaction(RT-PCR) and Western blot respectively.ResultsHigh performance liquid chromatography analysis demonstrated the amount of cellular total cholesterol were 76.28±10.36(A), 121.63±13.32(B), 136.23±14.78(C), 98.52±11.45(D) mg per gram protein.PPARγ antagonist GW9662 inhibited CD36 mRNA and protein synthesis.Ciglitazone increased CD36 mRNA and protein synthesis.The ratios of CD36/GAPDH were 0.78(A), 0.94(B), 1.12(C), 0.52(D) respectively.Western blot re-sults conform to RT-PCR outcomes. ConclusionAntagonist of PPARγ may decrease cholesterol accumulation and downregulate ox-LDL-induced CD36 expression in THP-1 macrophages.