Niacin Suppresses Progression of Atherosclerosis by Inhibiting Vascular Inflammation and Apoptosis of Vascular Smooth Muscle Cells

Background: Niacin is a broad-spectrum lipid-regulating drug used for the clinical therapy of atherosclerosis; however, the mechanisms by which niacin ameliorates atherosclerosis are not clear. Material/Methods: The effect of niacin on atherosclerosis was assessed by detection of atherosclerotic lesion area. Adhesion mol-ecules in arterial endothelial cells were determined by using qRT-PCR and Western blot analysis. The levels of serum inflammatory cytokines in ApoE–/ – mice were detected by using ELISA. We detected the expression levels of phosphorylated nuclear factors-kB (NF-kB) p65 in aortic endothelial cells of mice using Western blot analy-sis. Furthermore, we investigated the anti-inflammation effect and endothelium-protecting function of niacin and their regulatory mechanisms in vitro. Results: Niacin inhibited the progress of atherosclerosis and decreased the levels of serum inflammatory cytokines and adhesion molecules in ApoE–/ – mice. Niacin suppressed the activity of NF-kB and apoptosis of vascular smooth muscle cells (VSMCs). Furthermore, niacin induced phosphorylated focal adhesion kinase (FAK) and FAK inhib-itor PF-573228 reduced the level of Bcl-2 and elevated the level of cleaved caspase-3 in VSMCs. Conclusions: Niacin inhibits vascular inflammation and apoptosis of VSMCs via inhibiting the NF-kB signaling and the FA