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 [Go to this article.]

Figure 4
Effect of HIV protease inhibitors on plasma lipids. 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). The total plasma triglyceride (a) and cholesterol/cholesteryl ester (b) levels were determined after 0, 4, and 8 weeks of treatment with a commercial kit (Wako Chemicals USA Inc.) or gas chromatography. Bars represent mean ± SE, n = 8. *P < 0.01 compared with vehicle. White bars are vehicle controls, black bars are low-dose protease inhibitors, and gray bars are high-dose protease inhibitors.