Dexmedetomidine attenuates lipopolysaccharide induced acute lung injury by targeting NLRP3 via miR‐381

Abstract

Dexmedetomidine (Dex) is an agonist of α2-adrenergic receptors, and it is used as an anxiety reducing, sedative, and pain medication in clinical. Studies have shown that dexmedetomidine protects against lipopolysaccharide (LPS)-induced acute lung injury; however, the underlying mechanism is still unclear. To investigate, an acute lung injury mouse model was induced by intraperitoneal injection of LPS. Histopathological changes were determined by hematoxylin and eosin staining. Enzyme-linked immunosorbent assay was used to detect cytokines in serum. microRNA expression levels were detected by quantitative reverse transcription polymerase chain reaction. Protein levels were detected by western blot. Dex treatment significantly attenuated lung injury and inhibited the expression levels of the inflammation factors via reducing the level of NACHT, LRR, and PYD domains-containing protein 3 (NLRP3) and autocleavage of caspase-1. Moreover, mmu-miR-381, which targets the mRNA of NLRP3, was upregulated after Dex treatment. Dex attenuates LPS-induced acute lung injury via miR-381-targeted NLRP3.