Nifedipine inhibits apoptotic cell death of cultured endothelial cells induced by tumor necrosis factor-α

被引:0
|
作者
Yamagishi, S
Inagaki, Y
Abe, R
Kikuchi, S
Sasaki, N
Takeuchi, M
机构
[1] Kurume Univ, Sch Med, Dept Med, Kurume, Fukuoka 8300011, Japan
[2] Hokkaido Univ, Grad Sch Med, Dept Dermatol, Sapporo, Hokkaido, Japan
[3] Hokkaido Univ, Grad Sch Med, Dept Neurol, Sapporo, Hokkaido, Japan
[4] Sapporo Med Univ, Sch Med, Dept Neuropsychiat, Sapporo, Hokkaido, Japan
[5] Hokuriku Univ, Fac Pharm Sci, Dept Biochem, Kanazawa, Ishikawa, Japan
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D O I
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中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Impaired endothelial cell (EC) growth and function have been suggested to be an initial event that leads to the development of atherosclerosis. We have very recently found that nifedipine, one of the most popularly used dihydropyridine-based calcium antagonists, prevented EC monocyte chemoattractant protein-1 production elicited by tumor necrosis factor-alpha (TNF-alpha) through its antioxidative properties. However, the effects of nifedipine on EC growth and apoptosis are not fully understood. In this study, we investigated whether nifedipine could inhibit tumor necrosis factor (TNF)-alpha-induced growth retardation and apoptotic cell death in human umbilical vein ECs (HUVECs). TNF-alpha inhibited EC proliferation, which was significantly blocked by nifedipine or antioxidant N-acetylcysteine (NAC). Nifedipine or NAC was also found to significantly inhibit apoptotic cell death of TNF-alpha-exposed HUVECs. Our present study suggests that nifedipine may play a protective role against the development and progression of atherosclerosis by promoting EC repair through its antioxidative properties.
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页码:141 / 145
页数:5
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