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

Kyeong Min Lee, Keun Gyu Park, Yong Deuk Kim, Hyo Jung Lee, Hyoung Tae Kim, Won Hyun Cho, Hye Soon Kim, Seong Wook Han, Gou Young Koh, Joong Yeol Park, Ki Up Lee, Jung Guk Kim, In Kyu Lee

Research output: Contribution to journalArticlepeer-review

36 Scopus citations


Vascular inflammation induced by the proinflammatory cytokine/NF-κB 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 α-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-α-stimulated fractalkine expression in cultured vascular smooth muscle cells (VSMCs), a process which is mediated through the NF-κB pathway. In addition to fractalkine, ALA successfully inhibited TNF-α-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-κB/fractalkine pathway, may be used to prevent neointimal hyperplasia after angioplasty or stenting.

Original languageEnglish
Pages (from-to)106-114
Number of pages9
Issue number1
StatePublished - Nov 2006


  • α-Lipoic acid
  • Atherosclerosis
  • Fractalkine
  • Neointimal hyperplasia
  • NF-κB
  • Vascular smooth muscle cell


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