Niacin inhibits vascular oxidative stress, redox-sensitive genes, and monocyte adhesion to human aortic endothelial cells

Abstract In pharmacological doses, nicotinic acid (niacin) reduces myocardial infarction, stroke and atherosclerosis. The beneficial effects of niacin on lipoproteins are thought to mediate these effects. We hypothesized that niacin inhibits oxidative stress and redox-sensitive inflammatory genes th...

Full description

Saved in:
Bibliographic Details
Published in:Atherosclerosis 2009-01, Vol.202 (1), p.68-75
Main Authors: Ganji, Shobha H, Qin, Shucun, Zhang, Linhua, Kamanna, Vaijinath S, Kashyap, Moti L
Format: Article
Language:English
Subjects:
Aorta - cytology
Aortic endothelial cells
Atherosclerosis
Atherosclerosis (general aspects, experimental research)
Biological and medical sciences
Blood and lymphatic vessels
Blood vessels and receptors
Cardiology. Vascular system
Cardiovascular
Cell Adhesion
Cells, Cultured
Endothelial Cells - cytology
Endothelium, Vascular - drug effects
Endothelium, Vascular - pathology
Fundamental and applied biological sciences. Psychology
Glutathione
Glutathione - metabolism
Humans
LDL oxidation
Lipoproteins, LDL - metabolism
MCP-1
Medical sciences
Monocytes - cytology
Monocytes - metabolism
NADPH
Niacin
Niacin - pharmacology
Oxidation-Reduction
Oxidative Stress
Reactive Oxygen Species
Vascular Cell Adhesion Molecule-1 - metabolism
Vascular inflammation
Vasodilator Agents - pharmacology
VCAM-1
Vertebrates: cardiovascular system
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Abstract In pharmacological doses, nicotinic acid (niacin) reduces myocardial infarction, stroke and atherosclerosis. The beneficial effects of niacin on lipoproteins are thought to mediate these effects. We hypothesized that niacin inhibits oxidative stress and redox-sensitive inflammatory genes that play a critical role in early atherogenesis. In cultured human aortic endothelial cells (HAEC), niacin increased nicotinamide adenine dinucleotide phosphate (NAD(P)H) levels by 54% and reduced glutathione (GSH) by 98%. Niacin inhibited: (a) angiotensin II (ANG II)-induced reactive oxygen species (ROS) production by 24–86%, (b) low density lipoprotein (LDL) oxidation by 60%, (c) tumor necrosis factor α (TNF-α)-induced NF-κB activation by 46%, vascular cell adhesion molecule-1 (VCAM-1) by 77–93%, monocyte chemotactic protein-1 (MCP-1) secretion by 34–124%, and (d) in a functional assay TNF-α-induced monocyte adhesion to HAEC (41–54%). These findings indicate for the first time that niacin inhibits vascular inflammation by decreasing endothelial ROS production and subsequent LDL oxidation and inflammatory cytokine production, key events involved in atherogenesis. Initial data presented herein support the novel concept that niacin has vascular anti-inflammatory and potentially anti-atherosclerotic properties independent of its effects on lipid regulation.
ISSN:0021-9150
1879-1484
DOI:10.1016/j.atherosclerosis.2008.04.044