【摘要】 目的:探讨血管生成素-1(Ang-1)对脓毒症小鼠肺血管内皮屏障功能及血管内皮钙黏蛋白(VEcadherin)的影响及作用机制。方法:80只BALB/c小鼠随机分NS组、LPS组、LPS+Ang-1组、LPS+Ang-1+Ly组和Ang-1组(n=16)。测血浆VE-cadherin、Ang-2水平,肺湿干比,肺通透指数(LPI),检测肺总VEcadherin、磷酸化VE-cadherin。结果:除Ang-1组外各组血浆Ang-2较NS组均升高(P<0.01),LPS+Ang-1组和LPS+Ang-1+Ly组血浆Ang-2较LPS组降低(P<0.05),LPS+Ang-1+Ly组血浆Ang-2较LPS+Ang-1组明显升高(P<0.01)。肺湿干比、LPI、血浆VE-cadherin与肺磷酸化VE-cadherin变化趋势与Ang-2相同。肺总VE-cadherin变化趋势与Ang-2相反。结论:Ang-1可能通过PI3K/Akt信号通路调节脓毒症小鼠VE-cadherin从而改善肺血管内皮屏障功能。更多还原

【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 VEcadherin 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 PI3 K / Akt signal transduction pathway,Ang-1 may regulate septic mice′ VE-cadherin, hence the pulmonary vascular endothelial barrier function improved.更多还原