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Objective-The goal of this study was to investigate the effects of nonenzymatic glycation on the antiinflammatory properties of apolipoprotein (apo) A-I. Methods and Results-Rabbits were infused with saline, lipid-free apoA-I from normal subjects (apoA-I N ), lipid-free apoA-I nonenzymatically glycated by incubation with methylglyoxal (apoA-I Glyc in vitro ), nonenzymatically glycated lipid-free apoA-I from subjects with diabetes (apoA-I Glyc in vivo ), discoidal reconstituted high-density lipoproteins (

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Several known functions of high-density lipoproteins (HDLs) may contribute to their ability to protect against atherosclerosis. The best known of these functions is the ability to promote cholesterol efflux from cells in a process that may minimize the accumulation of foam cells in the artery wall. However, HDLs have additional properties, including antioxidant, anti-inflammatory, and antithrombotic effects, that may also be anti-atherogenic. Recent in vivo studies in several animal models have demonstrated that HDLs can inhibit acute and chronic vascular inflammation. The fact that these effects can be achieved with very low doses of reconstituted discoidal HDL or even lipid-free apolipoprotein A-I suggests that they may reflect activity of a minor, highly active HDL subpopulation. These results have potentially important clinical implications in regard to managing the acute vascular inflammation states that accompany acute coronary syndrome and acute ischemic stroke.

Objective-The purpose of this study was to investigate the ability of high-density lipoproteins (HDLs) to upregulate genes with the potential to protect against inflammation in endothelial cells. Methods and Results-Human coronary artery endothelial cells (HCAECs) were exposed to reconstituted HDLs (rHDLs) for 16 hours before being activated with tumor necrosis factor-␣ (TNF-␣) for 5 hours. rHDLs decreased vascular cell adhesion molecule-1 (VCAM-1) promoter activity by 75% (PϽ0.05), via the nuclear factor-kappa B (NF-B) binding site. rHDLs suppressed the canonical NF-B pathway and decreased many NF-B target genes. Suppression of NF-B and VCAM-1 expression by rHDLs or native HDLs was dependent on an increase in 3␤-hydroxysteroid-⌬24 reductase (DHCR24) levels (PϽ0.05).

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