Role of sphingosine 1-phosphate on high glucose-induced vascular endo-thelial cell dysfunction
10.3969/j.issn.1000-4718.2016.02.009
- VernacularTitle:1-磷酸鞘氨醇在高糖诱导血管内皮细胞功能损伤中的作用
- Author:
Weihua LIU
;
Shuangfeng LIN
;
Jixiang SHI
;
Ting PAN
;
Qiumei CHEN
;
Shuoting WANG
;
Hui SHANG
- Publication Type:Journal Article
- Keywords:
Sphingosine 1-phosphate;
Endothelial cells;
Endothelial nitric oxide synthase;
Intercellular adhe-sion molecule-1
- From:
Chinese Journal of Pathophysiology
2016;32(2):245-250
- CountryChina
- Language:Chinese
-
Abstract:
AIM:To explore the role of sphingosine 1-phosphate (S1P) in the dysfunction of vascular endo-thelial cells exposed to high glucose.METHODS: In human aortic endothelial cells cultured under high-glucose ( 22 mmol/L glucose) medium, nitric oxide ( NO) level, polymorphonuclear neutrophil-endothelial cell adhesion rate, protein level of intercellular adhesion molecule-1 ( ICAM-1) , migration of endothelial cells and Akt/endothelial nitric oxide syn-thase ( eNOS) pathway activation were observed after S1P, sphingosine kinase-1 inhibitor and/or Akt inhibitor treatments. RESULTS:S1P decreased NO level, increased polymorphonuclear neutrophil adhesive rate, enhanced ICAM-1 protein level, and inhibited migration of endothelial cells and activation of Akt/eNOS pathway in endothelial cells cultured under high-glucose condition.Sphingosine kinase-1 inhibitor, which reduced S1P content, significantly improved the above endo-thelial cell function indexes and restored the activation of Akt/eNOS pathway.CONCLUSION: S1P promoted high glu-cose-induced dysfunction of endothelial cells probably by inhibiting the activation of Akt/eNOS signal pathway.Targeting S1P is expected to become one of potential treatment strategies to reduce endothelial cell dysfunction.
