Abstract
Unrestrained inflammation provokes oxidative stress and contributes to the development of sepsis-induced acute lung injury (ALI). MicroRNA-326 (miR-326) is originally identified as an autoimmunity-associated microRNA, yet its role and potential molecular basis in sepsis-induced ALI remain unclear. Herein, we found that miR-326 was downregulated in murine lungs and macrophages upon lipopolysaccharide (LPS) stimulation. MiR-326 agomir prevented, whereas miR-326 antagomir exacerbated LPS-induced inflammation, oxidative stress, and ALI in mice. Furthermore, we found that miR-326 suppressed LPS-induced inflammation and oxidative stress in macrophages via downregulating toll-like receptor (TLR4), and TLR4 inhibition abolished miR-326 antagomir-mediated deleterious effect in vivo and in vitro. Finally, we proved miR-326 agomir notably alleviated sepsis-induced ALI after caecal ligation and puncture surgery. Our data identified miR-326 as a potential therapeutic target for sepsis-induced ALI.