CAJ | 학술논문

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（VE-cadherin ）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VE-cadherin、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。
목적：탐토혈관생성소-1（Ang-1）대농독증소서폐혈관내피병장공능급혈관내피개점단백（VE-cadherin ）적영향급작용궤제。방법：80지BALB/c 소서수궤분NS조、LPS 조、LPS＋Ang-1조、LPS＋Ang-1＋Ly조화Ang-1조（n＝16）。측혈장VE-cadherin、Ang-2수평，폐습간비，폐통투지수（LPI），검측폐총VE-cadherin、린산화VE-cadherin。결과：제Ang-1조외각조혈장Ang-2교NS조균승고（P＜0．01），LPS＋Ang-1조화LPS＋Ang-1＋Ly 조혈장Ang-2교LPS조강저（P＜0．05），LPS＋Ang-1＋Ly 조혈장Ang-2교LPS＋Ang-1조명현승고（P＜0．01）。폐습간비、LPI、혈장VE-cadherin여폐린산화VE-cadherin변화추세여Ang-2상동。폐총VE-cadherin변화추세여Ang-2상반。결론：Ang-1가능통과PI3K/Akt신호통로조절농독증소서VE-cadherin종이개선폐혈관내피병장공능。
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.