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

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.
AuthorsS Yamagishi, Y Inagaki, R Abe, S Kikuchi, N Sasaki, M Takeuchi
JournalDrugs under experimental and clinical research (Drugs Exp Clin Res) Vol. 29 Issue 4 Pg. 141-5 ( 2003) ISSN: 0378-6501 [Print] Switzerland
PMID15018304 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Calcium Channel Blockers
  • Free Radical Scavengers
  • Tumor Necrosis Factor-alpha
  • Nifedipine
  • Acetylcysteine
Topics
  • Acetylcysteine (pharmacology)
  • Apoptosis (drug effects)
  • Calcium Channel Blockers (pharmacology)
  • Cell Count
  • Cell Survival (drug effects)
  • Cells, Cultured
  • Endothelial Cells (drug effects)
  • Free Radical Scavengers (pharmacology)
  • Humans
  • Nifedipine (pharmacology)
  • Tumor Necrosis Factor-alpha (antagonists & inhibitors, pharmacology)

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