Korean J Physiol Pharmacol.
1997 Oct;1(5):515-521.
Nitric oxide prevents the bovine cerebral endothelial cell death
induced by serum-deprivation
- Affiliations
-
- 1Yonsei Brain Research Institute, Yonsei University College of Medicine, Seoul 120-752, South Korea.
- 2Department of Pharmacology, Yonsei University College of Medicine, Seoul 120-752, South Korea.
Abstract
-
Endothelial cells play a central role in the inflammatory processes,
and activation of nuclear factor kappa B (NF-kappaB) is a key component
in that inflammatory processes. Previously, we reported that tumor
necrosis factor alpha(TNF alpha) had protective effect on cell death
induced by serum deprivation and this protection was related to
NF-kappa B activation. Inducible nitric oxide synthase (iNOS) is a
member of the molecules which transcription is regulated mainly by
NF-kappa B. And the role of nitric oxide (NO) generated by iNOS on cell
viability is still controversial. To elucidate the mechanism of TNF a
and NF-kappa B 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 TNF a, 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 TNFalpha 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-kappa B exerts its cytoprotective effect.