To observe the role and mechanism of miR-138-5p in seawater aspiration-induced acute lung injury(ALI).

Rats and rat pulmonary vascular endothelial cells(RPMVECs) seawater aspiration induced ALI models were established and were divided into 4 groups: normal control group, seawater group, miR-138-5p antagomir group and antag NC pre-treated group. W/D ratio and Evans blue were carried out after modeling. The contents of tumor necrosis factor-α(TNF-α), interleukin-1β(IL-1β) and interleukin-6(IL-6) were measured by enzyme linked immunosorbent serologic assay(ELISA) and the expression of SIRT1 and Acetyl-nuclear factor kappa-B(NF-κB) were measured by western blot. Doubleluciferase reporter gene assay was used to verify the functional relationship between SIRT1 and miR-138-5p.

After 4 h seawater stimulation, W/D ratio and Evans blue were obvious and the contents of TNF-α, IL-1β and IL-6 were increased. The expression of miR-138-5p, Acetyl-NF-κB were increased and SIRT1 expression was inhibited. Inhibition of miR-138-5p decreased the inflammation, oxidative stress and Acetyl-NF-κB and increased the expression of SIRT1.

These results suggest that increased expression of miR-138-5p was an important cause in seawater-induced ALI and this phenomenon was through SIRT1 pathway.