Endogenous nitric oxide mediates lipoteichoic acid induced preconditioning on reoxygenation injury of cultured human coronary artery endothelial cells
- VernacularTitle:内源性一氧化氮介导脂质胞壁酸预适应对人冠脉内皮细胞再复氧损伤的作用
- Author:
Shiyu MA
;
Jizhou XIANG
;
Jiliang WU
;
Yexin MA
;
Benrong HU
- Publication Type:Journal Article
- Keywords:
lipoteichoic acid;
nitric oxide;
human coronary artery endothelial cells;
reoxygenation injury
- From:
Acta Pharmaceutica Sinica
2005;40(4):316-321
- CountryChina
- Language:Chinese
-
Abstract:
Aim To explore the effects of lipoteichoic acid (LTA) induced delayed preconditioning (PC) on hypoxia-reoxygenation (H/R) injury of cultured human coronary artery endothelial cells (HCAECs), and to investigate the potential role of endogenous nitric oxide (NO) participated in the protective mechanism. Methods HCAECs were incubated for 2 h in a hypoxic atmosphere and reoxygenated for 4 h in a normoxic atmosphere. The delayed PC was induced by pretreatment with LTA assessed by the percentage of cellular injury with Trypan blue exclusion and by the amount of lactate dehydrogenase (LDH) in culture media. The NO level of the culture media was measured detect the expression of eNOS mRNA by RT-PCR method after cells were recovered from different points.Results LTA pretreatment significantly decreased the percentage of the killed cell and the concentration of LDH in media. Also, LTA pretreatment obviously raised the concentrations of NO in culture media. The protective effects of LTA were abrogated by pretreatment with N-monomethyl-L-arginine (L-NMMA).Moreover, the expression of eNOS mRNA was significantly upregulated after HCAECs exposure to LTA for 4 h following 2 h or 4 h recovery. Conclusion LTA could induce the delayed protection against H/R induced endothelial injury and dysfunction of cultured HCAECs. NO produced by eNOS acts initially as a trigger and subsequently as a mediator of delayed PC.
