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.