Upregulation of miRNA-140-5p inhibits inflammatory cytokines in acute lung injury through the MyD88/NF-κB signaling pathway by targeting TLR4.

Abstract

The present study was designed to determine the effect of miR-140-5p on acute lung injury (ALI) and the associated inflammation induced. As a result, miR-140-5p expression in mice with ALI was suppressed when compared with the normal group. Downregulation of miR-140-5p increased the levels of inflammatory factors induced by ALI [including tumor necrosis factor-α, interleukin (IL)-1β, IL-6 and myeloperoxidase] in an in vitro model of human lung A549 cells. Downregulation of miR-140-5p also induced the protein expression of Toll-like receptor 4 (TLR4), myeloid differentiation primary response 88 (MyD88) and nuclear factor (NF)-κB in an in vitro model. Overexpression of miR-140-5p reduced the levels of inflammation in the in vitro model of ALI via the suppression of the TLR4/MyD88/NF-κB signaling pathway. The inhibition of TLR4 using a TLR4 inhibitor reduced the proinflammation effects of anti-miR-140-5p in the in vitro model of ALI. The NF-κB inhibitor also inhibited the proinflammation effects of anti-miR-140-5p in the in vitro model of ALI. Overall, the results of the present study indicated that miR-140-5p inhibited ALI-induced inflammation via the TLR4/MyD88/NF-κB signaling pathway.