Protective Effect of Nitric Oxide Against Lipopolysaccharide-induced Cytotoxicity in C6-glial Cell.
- Author:
Ho Geun HWANG
1
;
Jung Mu HER
;
Hyun Ju BANG
;
Bum Young KIM
;
Hong Moon SOHN
;
Yeun Ja MUN
;
Jay Min OH
;
Yeun Tai CHUNG
;
Min Kyu CHOI
Author Information
1. Department of Anatomy School of Medicine, Wonkwang University, Iksan, Korea.
- Publication Type:Original Article
- Keywords:
Nitric oxide (NO);
Lipopolysaccharide (LPS);
NF-kB;
C6 glial cells;
Caspase-3
- MeSH:
Brain;
Caspase 3;
Cell Death;
Neuroglia;
NF-kappa B;
Nitric Oxide*;
Nitroprusside
- From:Korean Journal of Anatomy
2000;33(5):579-586
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Nitric oxide (NO) is mainly involved in brain ischemic damage to elucidate the protective mechanism of NO pretreatment on ischemic-induced cytotoxicity. This study was investigated whether NO pretreatment inhibits the increase of iNOS expression by lipopolysaccharide (LPS) combined phorbol 12-myristate 13-acetate (PMA) via regulating NF-kB activation in C6 glial cells. C6 glial cells with LPS and PMA for 72 hours markedly induced NO, but sodium nitroprusside (SNP) (100 nM) pretreatment before exposure of LPS and PMA significantly supressed NO production, iNOS expression and NF-kB activation by LPS and PMA. In addition, LPS and PMA treatment for 72 hours induced severely cell death and LDH release from cell into media in C6 glial cells. However SNP pretreatment before treatment of LPS and PMA significantly protected LPS and PMA induced cytotoxicity. Treatment with LPS and PMA induced caspase 3 activation follewed by chromosomal condensation, and fragmentation of nuclei in C6 glial cells. SNP pretreatment before exposure to LPS and PMA supressed caspase 3 activation and inhibited chromosomal condensation and fragmentation of nuclei. From these above results, it is suggest that the protective effects of SNP pretreatment against LPS and PMA induced cytotoxicity may be mediated by inhibiting the expression of iNOS via regulating NF-kB activation.
