MicroRNA-217 modulates inflammation, oxidative stress, and lung injury in septic mice via SIRT1.

Inflammation and oxidative stress contribute to the initiation and progression of septic lung injury. MicroRNA-217 () is proved to be involved in controlling inflammatory response and oxidative stress, yet its role and underlying mechanism in the pathogenesis of septic lung injury remain elusive. Caecal ligation and puncture surgery were performed to generate sepsis and mice were kept for 12 h to imitate septic lung injury. Next, mice were administrated with antagomir or agomir to decrease or increase the expression of in lung tissue. Moreover, primary peritoneal macrophages were separated and incubated with lipopolysaccharide (LPS) to further verify the role of . was upregulated in septic lungs and primary macrophages. antagomir alleviated, whereas agomir aggravated inflammation and oxidative stress in septic mice and LPS-stimulated macrophages. Further detection identified SIRT1 was responsible for antagomir-mediated anti-inflammatory and anti-oxidant effects, and SIRT1 inhibition abolished the beneficial effects of antagomir and . Our data defined as a therapeutic target for treating septic lung injury.