Twenty C57BL/6J mice were randomly divided into control group and LPS group， and there were 10 mice in each group. After treatment， the mouse samples were obtained. HE staining was used to observe the pathomorphology of lung tissue of the mice in two groups， RT-PCR method and Western blotting method were used to detect the expression levels of α-subunit ENaC（αENaC） mRNA and pFOXO1 （Ser256） protein in lung tissue of the mice in two groups.The alveolar epithelial A549 cells were cultured， and then infected with ADV-FOXO1 or shRNA-FOXO1， respectively.RT-PCR method was used to determine the expression of αENaC mRNA. The A549 cells were divided into control group， insulin group， insulin+PI3K inhibitor group， and insulin+AKT inhibitor group. After corresponding intervention， Western blotting method was used to detect the expression levels of pFOXO1 （Ser256） protein，RT-PCR method was used to determine the expression levels of αENaC mRNA， and immunofluorescence method was used to detect the intracellular localization of FOXO1.

Compared with control group， the lung injury score of mice in LPS group was increased significantly （P<0.05）， the expression levels of pFOXO1 （Ser256） and αENaC proteins in the lung tissue were significantly decreased（P<0.05） and they showed positively correlated relationship（r=0.703， P<0.05）.Compared with control group； the expression level of αENaC mRNA in A549 cells in over-expression FOXO1 group was significantly decreased （P<0.05），and the expression level of αENaC mRNA in silencing FOXO1 group was significantly increased（P<0.05）； compared with control group， the expression levels of pFOXO1 protein and αENaC mRNA in the A549 cells in insulin group were increased significantly （P<0.05）， and FOXO1 was mainly located in the cytoplasm. The expression levels of αENaC mRNA and pFOXO1 protein in A549 cells in insulin+PI3K inhibitor group and insulin+AKT inhibitor group were lower than those in insulin group （P<0.05）.

After inactiviation of FOXO1 phosphorylation，FOXO1 can translocate from nucleus to cytoplasm to weaken the inhibitory effect of αENaC and upregulate the expression of αENaC.