HIV protease inhibitors promote atherosclerotic lesion formation independent of dyslipidemia by increasing CD36-dependent cholesteryl ester accumulation in macrophages
J. Clin. Invest. James Dressman, et al. 111:389 doi:10.1172/JCI16261 [
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Figure 5HIV protease inhibitors induce an increase in peritoneal macrophage cholesterol/cholesteryl ester levels. Six-week-old male LDLR null mice on a chow diet were given vehicle control (0.01% ethanol) or the following protease inhibitors in their drinking water: amprenavir (23 or 75 μg/mouse/day), indinavir (25 or 75 μg/mouse/day), or ritonavir (10 or 50 μg/mouse/day). After 8 weeks of treatment, peritoneal macrophages were isolated and cholesterol/cholesteryl ester mass was determined by gas chromatography. Bars represent mean ± SE,
n = 8. *
P < 0.01 compared with vehicle,
#P < 0.01 compared with low dose of the same protease inhibitor.