Vascular endothelial barrier dysfunction is the most prominent manifestation and important cause of mortality in infectious acute lung injury (ALI). Exogenous apelin is effective in ameliorating lipopolysaccharide (LPS)-induced inflammatory response in ALI lungs, reducing exudation of lung tissue and decreasing mortality. This study set out to investigate the association between apelin and Friend leukemia integration-1 (Fli-1) in the prevention and treatment of ALI, and to elucidate the molecular mechanism by which apelin protects the permeability of the vascular endothelial barrier. At the vivo functional level, lung wet/dry weight ratio was used to detect whole lung permeability, evans blue assay and dual fluorescent protein tracking assay were used to detect lung vascular endothelial permeability, HE staining to observe the inflammatory status of lung tissue, and immunofluorescence staining for VE-cadherin expression levels in blood vessels. The changes in inflammatory factors in bronchoalveolar lavage fluid (BALF) were detected by ELASA. Western blot was used to detect the expression level of proteins. qRT-PCR was performed to detect changes in mRNA expression of Fli-1 and adherent junction-related proteins. The correlation analysis of Fli-1 with vascular endothelial permeability and SRC showed that Fli-1 participated in the process of ALI. After preventive and therapeutic treatment of ALI mice with exogenous apelin, Fli-1, APJ, VE-cadherin, phosphorylated-VE-cadherin (p-VE-cadherin) and β-catenin were up-regulated, while SRC, phosphorylated-SRC (p-SRC), VEGF and VEGF-R were down-regulated, which indicated that the stability of vascular endothelial barrier was enhanced. With the use of Fli-1 inhibitor irinotecan, the protective effect of apelin was weakened in various functional indexes, genes and proteins. The lung was maintained at the level of the injury. Our research shows that Fli-1 is involved in the LPS-induced ALI process. The molecular mechanism for apelin in preventing endothelial barrier dysfunction in ALI is through up-regulating Fli-1, thus regulating adherens junction-related proteins, and finally recovering the endothelial barrier function.

血管内皮屏障功能障碍是感染性急性肺损伤（ALI）最突出的表现和重要的死亡原因。外源性 Apelin 可有效改善 ALI 肺部脂多糖 (LPS) 诱导的炎症反应，减少肺组织渗出并降低死亡率。本研究旨在探讨apelin与Friend leukemia integration-1 (Fli-1)在ALI防治中的关系，阐明apelin保护血管内皮屏障通透性的分子机制。在体内功能水平，肺湿/干重比用于检测全肺通透性，伊文思蓝法和双荧光蛋白跟踪法用于检测肺血管内皮通透性，HE染色观察肺组织炎症状态，免疫荧光染色观察血管VE-cadherin表达水平。ELASA检测支气管肺泡灌洗液（BALF）中炎症因子的变化。Western blot用于检测蛋白的表达水平。进行 qRT-PCR 以检测 Fli-1 和粘附连接相关蛋白的 mRNA 表达变化。Fli-1与血管内皮通透性、SRC的相关性分析表明Fli-1参与了ALI的过程。外源性apelin防治ALI小鼠后，Fli-1、APJ、VE-cadherin、磷酸化VE-cadherin（p-VE-cadherin）和β-catenin表达上调，而SRC、phosphorylated-SRC（ p-SRC)、VEGF 和 VEGF-R 被下调，这表明血管内皮屏障的稳定性增强。随着Fli-1抑制剂伊立替康的使用，apelin在各项功能指标、基因和蛋白质方面的保护作用减弱。肺保持在受伤的水平。我们的研究表明 Fli-1 参与了 LPS 诱导的 ALI 过程。Apelin预防ALI内皮屏障功能障碍的分子机制是通过上调Fli-1，从而调节粘附连接相关蛋白，最终恢复内皮屏障功能。我们的研究表明 Fli-1 参与了 LPS 诱导的 ALI 过程。Apelin预防ALI内皮屏障功能障碍的分子机制是通过上调Fli-1，从而调节粘附连接相关蛋白，最终恢复内皮屏障功能。我们的研究表明 Fli-1 参与了 LPS 诱导的 ALI 过程。Apelin预防ALI内皮屏障功能障碍的分子机制是通过上调Fli-1，从而调节粘附连接相关蛋白，最终恢复内皮屏障功能。