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

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

Abstract

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 molecules 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-κB (NF-κB) p65 in aortic endothelial cells of mice using Western blot analysis. 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-κB and apoptosis of vascular smooth muscle cells (VSMCs). Furthermore, niacin induced phosphorylated focal adhesion kinase (FAK) and FAK inhibitor 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-κB signaling and the FAK signaling pathway, respectively, thus protecting ApoE−/− mice against atherosclerosis.

MeSH Keywords: Apoptosis, Atherosclerosis, Inflammation Mediators, Niacin

Authors: Gang Su,1,A,D,E,F,* Guangli Sun,2,A,D,E,F,G,* Hai Liu,1,B,C,D Liliang Shu,1,B,C,D Jingchao Zhang,1,B,C,DLonghui Guo,1,B,C,F Chen Huang,1,B,C,F and Jing Xu1,B,C,F

Influence Factor: 1.585

Citation: Med Sci Monit 21, 4081-4089 (2015).

Read entire article

Share:

Back to top