and assessment of the protective effect of sufentanil in acute lung injury.

OBJECTIVES

To investigate the mechanisms underlying the protective effect of sufentanil against acute lung injury (ALI).

MATERIAL AND METHODS

Rats were administered lipopolysaccharide (LPS) by endotracheal instillation to establish a model of ALI. LPS was used to stimulate BEAS-2B cells. The targets and promoter activities of IκB were assessed using a luciferase reporter assay. Apoptosis of BEAS-2B cells was evaluated by terminal deoxynucleotidyl transferase dUTP nick end labeling.

RESULTS

Sufentanil treatment markedly reduced pathological changes in lung tissue, pulmonary edema and secretion of inflammatory factors associated with ALI and . In addition, sufentanil suppressed apoptosis induced by LPS and activated NF-κB both and . Furthermore, upregulation of high mobility group box protein 1 (HMGB1) protein levels and downregulation of miR-129-5p levels were observed and following sufentanil treatment. miR-129-5p targeted the 3' untranslated region and its inhibition decreased promoter activities of IκB-α. miR-129-5p inhibition significantly weakened the protective effect of sufentanil on LPS-treated BEAS-2B cells.

CONCLUSION

Sufentanil regulated the miR-129-5p/HMGB1 axis to enhance IκB-α expression, suggesting that sufentanil represents a candidate drug for ALI protection and providing avenues for clinical treatment.