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Alpha-lipoic acid inhibits fractalkine expression and prevents neointimal hyperplasia after balloon injury in rat carotid artery

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Author(s)
박근규김혜순한성욱김형태조원현
Alternative Author(s)
Park, Keun GyuKim, Hye SoonHan, Seong WookKim, Hyoung TaeCho, Won Hyun
Publication Year
2006
Abstract
Vascular inflammation induced by the proinflammatory cytokine/NF- B pathway is one of the key mechanisms in the development of
neointimal hyperplasia. Accumulating evidence suggests that a recently identified chemokine, fractalkine, is involved in arterial inflammation
and atherogenesis. However, no study has examined the expression of neointimal fractalkine and the effects of pharmacological agents on this
process. The purposes of this study were to measure neointimal fractalkine expression in the rat carotid artery following balloon injury and to
determine if -lipoic acid (ALA) inhibits fractalkine expression and neointimal hyperplasia. Balloon injury of the rat carotid artery induced
fractalkine expression in the medial as well as neointimal regions. ALA inhibited this expression and consequently prevented neoinitmal
hyperplasia in a balloon-injured rat carotid artery. Additionally, ALA inhibited TNF- -stimulated fractalkine expression in cultured vascular
smooth muscle cells (VSMCs), a process which is mediated through the NF- B pathway. In addition to fractalkine, ALA successfully
inhibited TNF- -stimulated expression of vascular cell adhesion molecule-1 and monocyte chemotactic protein-1 in cultured VSMCs. These
data suggest that the cytokine–fractalkine system is involved in the pathogenesis of restenosis. The present study supports the possibility that
ALA, which inhibits the NF- B/fractalkine pathway, may be used to prevent neointimal hyperplasia after angioplasty or stenting.
© 2005 Elsevier Ireland Ltd. All rights reserved.
Keywords: -Lipoic acid; Atherosclerosis; Fractalkine; Neointimal hyperplasia; NF- B; Vascular smooth muscle cell
Department
Dept. of Internal Medicine (내과학)
Dept. of Surgery (외과학)
Publisher
School of Medicine
Citation
Atherosclerosis, Vol.189(1) : 106-114, 2006
Type
Article
ISSN
0021-9150
DOI
10.1016/j.atherosclerosis.2005.12.003
URI
http://kumel.medlib.dsmc.or.kr/handle/2015.oak/35134
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