Effect of Ang-1 on pulmonary VE-cadherin and barrier function in septic mice
10.3969/j.issn.1006-5725.2014.16.004
- VernacularTitle:血管生成素-1对脓毒症小鼠肺血管内皮钙黏蛋白及屏障功能的影响
- Author:
Zhenhua MAI
;
Xiuming ZHONG
;
Yuanli ZHANG
;
Huijuan HE
;
Huaguo YAO
;
Liehua DENG
;
Yunming CHEN
- Publication Type:Journal Article
- Keywords:
Sepsis;
Angiopoietin-1;
Vascular endothelial cadherin;
Phosphatidylinositol 3-kinase
- From:
The Journal of Practical Medicine
2014;(16):2535-2537
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the impact of Ang-1 on the septic mice′pulmonary vascular endothelial barrier function and VE-cadherin and its mechanism. Methods 80 BALB/c mice were randomly divided into NS, LPS, LPS+Ang-1, LPS+Ang-1+ Ly and Ang-1 groups (n = 16). Measure VE-cadherin, Ang-2 levels in plasma and lung permeability index (LPI).Test the total VE-cadherin of lung and the phosphorylation of VE-cadherin expression. Results Plasma Ang-2 was higher compared with NS group(P<0.01) except Ang-1 group. In LPS+Ang-1 group and LPS+Ang-1+Ly group, plasma Ang-2 was lower compared with LPS group (P <0.05). In LPS+Ang-1+Ly group, plasma Ang-2 was higher compared with LPS+Ang-1 group (P<0.01). LPI, plasma VE-cadherin and lung phosphorylation of VE-cadherin were the same with the trends of the plasma Ang-2 , but the lung total VE-cadherin showed the opposite tendency. Conclusion Through the PI3K/Akt signal transduction pathway , Ang-1 may regulate septic mice′VE-cadherin , hence the pulmonary vascular endothelial barrier function improved.
