Abstract: Abstract:Objective To investigate the role of PI3K/Akt signaling pathway on expression of alveolar epithelial sodium channel(ENaC) in LPS-induced acute lung injury (ALI). Methods Healthy adult Sprague-Dawley (SD) rats were randomly divided into control group, ALI group(LPS) ,treatment group(LPS+insulin), intervention group(LPS+insulin+wortmannin) with 5 rats in each group. The pathological changes in lung were observed, total lung water content(TLW) were measured, bronchoalveolar lavage fluid(BALF) were collected,and the mRNA and protein levels of ENaC and level of p-Akt were determined by RT-PCRand Western blot. Results Protein level and MPO activity in BALF and TLW in treatment group was significantly lower than that in ALI group (p＜0.05); Protein level and MPO activity in BALF and TLW in intervention group was significantly higher than that in treatment group (p＜0.05). The mRNA and protein levels of ENaC and level of p-Akt in treatment group were significantly higher than that of ALI group (p＜0.05); The mRNA and protein levels of ENaC and level of p-Akt in intervention group were significantly lower than that of treatment group (p＜0.05). Conclusion Activation of PI3K/Akt signaling pathway up-regulates the expression of ENaC to clear the pulmonary edema fluid.

Key words: actue lung injury, epithelial sodium channel, PI3K/Akt signaling pathway