Dexmedetomidine Inhibits Acute Lung Injury by Upregulating miR-144 Expression in Mice

Abstract

The understanding of lung injury’s mechanisms at the molecular level is not fully completed. MicroR-NAs (miRNAs), which are part of different pathophysiological processes, are essential biological regulators that operate by suppressing target genes. A mouse model of acute lung injury (ALI), which is triggered by lipopolysaccharide (LPS), was used to analyze miR-144 level in the ALI mice with or without dexmedetomidine treatment. Inflammation was investigated by the ratio of wet weight’s value to dry weight (W/D) of the lung, the release of cytokines TNF-α, cytokines IL-6, and cytokines IL-1β, and MPO activity. To validate the effect of dexmedetomidine on miR-144, overex-pression and knockdown of miR-144 were applied to treat antagomir144 and agomir144. The result suggested that LPS-triggered ALI was alleviated by dexmedetomidine. miR-144 was downregulated in ALI mice. The knockdown of miR-144 attenuated the protection of dexmedetomidine to acute lung injury. Overexpression of miR-144 attenuated the ALI, which was induced by LPS.