Anti-inflammatory effects of microRNA-223 on sepsis-induced lung injury in rats by targeting the Toll-like receptor signaling pathway

The aim of the present study was to investigate the mediation of micro RNA (miR)-223 on the anti-inflammatory effect of the Toll-like receptor (TLR) signaling pathway on sepsis-induced lung injury in rats via negatively regulating the expression of interleukin (IL)-6. Sprague-Dawley rats were used in the present study. It was determined whether miR-223 is differentially expressed in the lung using reverse transcription-quantitative PCR techniques and the content of cytokines in bronchoalveolar lavage (BAL) fluid was detected. The protein expression levels of TLR4 and nuclear factor (NF)-kappa B p65 were examined by western blotting and the pathological changes in the lung tissues of the sepsis group were observed. Hematoxylin and eosin was used to stain the lung tissues. The alveoli in the sham group exhibited a normal structure and morphology. In the sepsis group, the alveoli of the lung tissues were surrounded by numerous neutrophils, the mesenchyme was swollen, regions of the alveolar wall exhibited fibrosis and the alveolar wall was thickened. Furthermore, in the sepsis group, miR-223 expression was increased in the lung tissues when compared with that in the sham group. The content of cytokines, IL-6 and IL-1 beta in the BAL fluid was significantly increased when compared with that of the sham group and TLR4 and NF-kappa B were also highly expressed. In addition, when compared with RAW264.7 cells that were overexpressing miR-223, the content of IL-6 and IL-1 beta in the supernatant and protein expression of TLR and NF-kappa B in cells were markedly decreased. Thus, it was demonstrated that miR-223 negatively regulated the expression of IL-6, mediating the TLR4/NF-kappa B signaling pathway and exerting an anti-inflammatory effect in sepsis-induced lung injury.