Figure 2.

SAA enhanced atherosclerosis and induced early pro-atherogenic changes in VCAM-1 staining in the aortae of ApoE⁻/⁻ mice, which can be prevented by HDL. Male ApoE⁻/⁻ mice were randomly allocated into 4 treatment arms and administered with vehicle (control), LPS, SAA alone, or SAA in combination with HDL, as described in the methods section. Mice were sacrificed at 4 weeks, hearts perfused with PBS (50 mM, pH 7.4), then harvested. Thoracic aortae attached to the dorsal third of each heart fixed were processed for immune histological analysis. Thin sections of thoracic aorta from mice designated to the control (panel A), LPS (B), SAA (C) groups, as well as mice pretreated with freshly isolated human HDL for 2 weeks prior to SAA administration (D) were incubated with anti-VCAM-1 and imaged by light microscopy (left column). Black arrows indicate the endothelial surface on the inner lumen of the artery in panels (A–D). Dark stained immuno-reactive VCAM-1 on the vascular endothelium is evident in Panel C, whereas it is markedly lower or absent in Panels A, B, and D. The panels in the right column (E–H) show a high-magnification view of corresponding boxed regions of endothelial with VCAM-1⁺ immuno-reactivity seen as a granular deposit on the endothelium. Data are representative of at least 3 fields of view from each section from control (n = 6 mice), LPS (n = 6), SAA (n = 6), and HDL/SAA (n = 6).