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

S Yamagishi, Y Inagaki, R Abe, S Kikuchi, N Sasaki, M Takeuchi
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Abstract

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.

硝苯地平抑制肿瘤坏死因子α诱导的内皮细胞凋亡。
内皮细胞(EC)生长和功能受损被认为是导致动脉粥样硬化发展的初始事件。我们最近发现硝苯地平,最常用的二氢吡啶钙拮抗剂之一,通过其抗氧化特性阻止肿瘤坏死因子- α (tnf - α)引起的EC单核细胞化学引诱蛋白-1的产生。然而,硝苯地平对EC生长和凋亡的影响尚不完全清楚。在这项研究中,我们研究硝苯地平是否能抑制肿瘤坏死因子(TNF)- α诱导的人脐静脉内皮细胞(HUVECs)生长迟缓和凋亡细胞死亡。tnf - α抑制EC增殖,硝苯地平或抗氧化剂n -乙酰半胱氨酸(NAC)可显著阻断EC增殖。硝苯地平或NAC也能显著抑制tnf α暴露的huvec的凋亡细胞死亡。我们目前的研究表明,硝苯地平可能通过其抗氧化特性促进EC修复,从而对动脉粥样硬化的发生和进展起保护作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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