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