The cytotoxicity of nitric oxide induced by inflammatory cytokine in combination with LPS in endothelial cells
- VernacularTitle:炎性细胞因子及脂多糖诱导产生的一氧化氮对人血管内皮细胞的损伤作用
- Author:
Zhixu HE
;
Tongfu ZHOU
;
Qingkui LIAO
;
Xueju XU
;
Chunhua LUO
;
Qinbo LI
;
Shuren WANG
;
Fengy LI
- Publication Type:Journal Article
- Keywords:
Nitric Oxide;
Cytokines;
Lipopolysaccharides;
Endothelium;
Cells
- From:
Chinese Journal of Pathophysiology
1999;0(09):-
- CountryChina
- Language:Chinese
-
Abstract:
AIM: To explore the mechanism underlying inducible nitric oxide (NO) caused injury of endothelial cells during inflammation. METHODS: The activity of iso-enzymes of NO synthase (NOS), NO level and iNOS expression were examined using NADPH method, Griess reaction and RT-PCR, respectively. Furthermore, the lactate dehydrogenase (LDH) release rate, malondialdehyde (MDA) content were also measured. RESULTS:Co-administration of cytokines (TNF-? 5?10 5 U/L, IL-1? 2?10 5 U/L, INF-? 2?10 5 U/L) and LPS (10 mg/L) caused an obvious increase in NOS activity, NO levels (about two-fold) and a significant injury of the cells. At the same time, a significant increase in iNOS mRNA was also detected. Wheareas, treatment of the cells separately with cytokines or LPS for 24 h had no significant effect on NOS activity and NO level in cell lysates, however, it caused a significant increase in LDH release and MDA content. Also, the effect of cytokines and LPS on cell viability was concentration-and time-dependent. L-NMMA, a inhibitor of NOS, can suppress inducible NO production and protect cells against NO induced injury. CONCLUSION:Co-administration of cytokines (TNF-?, IL-1? and INF-?) and LPS significant activated iNOS and NO production which, in turn, induced oxidative reaction in endothelial cells.
