کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2893767 1172420 2009 8 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Niacin inhibits vascular oxidative stress, redox-sensitive genes, and monocyte adhesion to human aortic endothelial cells
موضوعات مرتبط
علوم پزشکی و سلامت پزشکی و دندانپزشکی کاردیولوژی و پزشکی قلب و عروق
پیش نمایش صفحه اول مقاله
Niacin inhibits vascular oxidative stress, redox-sensitive genes, and monocyte adhesion to human aortic endothelial cells
چکیده انگلیسی

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.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Atherosclerosis - Volume 202, Issue 1, January 2009, Pages 68–75
نویسندگان
, , , , ,