Objective      To investigate the effect of rosiglitazone on cholesterol content and the expression of acyl-coenzyme A cholesterol acyltransferase 1 (ACAT1) and ATP-binding cassette transporter A1 (ABCA1) in RAW264.7 macrophage-derived foam cells

and to explore the mechanism of rosiglitazone in foam cell formation.       Methods      Mouse macrophage RAW264.7 cells were cultured in high-glucose DMEM and were randomly divided into a control group

an oxidized low-density lipoprotein (oxLDL) group

in which cells were incubated with 30 mg/L oxLDL for 48 h

and an oxLDL+rosiglitazone group

in which cells were incubated with 30 mg/L oxLDL plus 5

10 and 20 μmol/L rosiglitazone for 48 h

respectively (n=10). The formation of foam cells were identified by oil red O staining. The levels of intracellular total cholesterol (TC) and free cholesterol (FC) in each group were determined by a cholesterol detection kit

and the expression of ACAT-1 and ABCA-1 protein was determined by Western blotting.       Results      Mouse macrophage RAW264.7 cells in the oxLDL group were stained by oil red O

but the color of the macrophages in the oxLDL+rosiglitazone group was lighter than that in the oxLDL group. Compared with the oxLDL group

the contents of intracellular TC and FC in the oxLDL+rosiglitazone group significantly decreased (P0.05) in a dose-dependent manner. Western blot results showed the expression levels of ACAT-1 in the oxLDL+rosiglitazone group with different concentrations of rosiglitazone (5

10 and 20 μmol/L) were (0.94±0.11)

(0.86±0.13) and (0.58±0.12)

respectively

which were significantly different from that in the oxLDL group (1.19±0.12) (P0.05). The expression levels of ABCA-1 in the oxLDL+rosiglitazone group with different concentrations of rosiglitazone (5

10 and 20 μmol/L) were (0.72±0.08)

(0.91±0.15) and (1.15±0.11)

respectively

which were also significantly different from that in the oxLDL group (0.63±0.05) (P0.05).       Conclusion      Rosiglitazone may inhibit foam cell formation by decreasing the expression of ACAT-1 and increasing the expression of ABCA-1

which plays an important role in inhibiting atherosclerosis.