MicroRNAs are dysregulated in sepsis. Acute lung injury is a progressive syndrome during sepsis. However, the role of miR-129-5p in the development of acute lung injury induced by sepsis remains unclear.
The acute lung injury of sepsis model was established by cecal ligation puncture (CLP)-treated mice and lipopolysaccharide (LPS)-treated murine alveolar epithelial cell line (MLE)-12 cells. The lung injury in vivo was investigated by hematoxylin and eosin staining, terminal dexynucleotidyl transferase (TdT)-mediated dUTP nick end labeling staining, enzyme-linked immunosorbent assay, lung wet-to-dry weight ratio, and myeloperoxidase activity. The lung injury in vitro was evaluated by 3-(4,5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide, flow cytometry, and enzyme-linked immunosorbent assay. The expression levels of miR-129-5p and high mobility group box 1 (HMGB1) were measured by quantitative real-time polymerase chain reaction and Western blot. The association between miR-129-5p and HMGB1 was validated by luciferase assay and RNA immunoprecipitation.
The expression of miR-129-5p was decreased in CLP model and LPS-treated MLE-12 cells. Overexpression of miR-129-5p attenuated inflammatory response, apoptosis, lung wet/dry weight ratio, and myeloperoxidase activity induced by CLP surgery in vivo. Moreover, addition of miR-129-5p increased cell viability and suppressed cell apoptosis and inflammatory response in vitro. HMGB1 as a target of miR-129-5p alleviated miR-129-5p-mediated injury suppression in LPS-treated MLE-12 cells.
miR-129-5p protects against sepsis-induced acute lung injury by decreasing HMGB1 expression, providing new target for sepsis treatment.

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