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KMID : 0811719970010050515
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Korean Journal of Physiology & Pharmacology
1997 Volume.1 No. 5 p.515 ~ p.521
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Nitric Oxide Prevents the Bovine Cerebral Endothelial Cell Death Induced by Serum-Deprivation
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Chul Hoon Kim
Young Soo Ahn/Chul Hoon Kim/Young Soo Ahn
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Abstract
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Endothelial cells play a central role in the inflammatory processes, and activation of nuclear factor kappa B (NF?κB) is a key component in that inflammatory processes. Previously, we reported that tumor necrosis factor alpha(TNFα) had protective effect of cell death induced by serum deprivation and this protection was related to NF?κB activation. Inducible nitric oxide synthase (iNOS) is a member of the molecules which transcription is regulated mainly by NF?κB. And the role of nitric oxide (NO) generated by iNOS on cell viability is still controversial. To elucidate the mechanism of TNFα and NF?κB activation on cell death protection, we investigate the effect of NO on the cell death induced by serum- deprivation in bovine cerebral endothelial cells in this study. Addition of TNFα, which are inducer of iNOS, prevented serum-deprivation induced cell death. Increased expression of iNOS was confirmed indirectly by nitrite measurement. When selective iNOS inhibitors were treated, the protective effect of TNFα on cell death was partially blocked, suggesting that iNOS expression was involved in controlling cell death. Exogenously added NO substrate (L-arginine) and NO donors (sodium nitroprusside and S-nitroso-N-acetylpenicillamine) also inhibited the cell death induced by serum deprivation. These results suggest that NO has protective effect on bovine cerebral endothelial cell death induced by serum-deprivation and that iNOS is one of the possible target molecules by which NF?κB exerts its cytoprotective effect.
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KEYWORD
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TNF α, Endothelial cell death, iNOS, NO, NF-kB,
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