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Updated: Nov 29, 2025
Bronchoalveolar Lavage Exosomes in Lipopolysaccharide-induced Septic Lung Injury
Published on: May 21, 2018
MicroRNA-217 modulates inflammation, oxidative stress, and lung injury in septic mice via SIRT1
Jie Yan1, Fan Yang1, Dengyun Wang1
1Department of Thoracic and Cardiovascular Surgery, Huangshi Central Hospital (Affiliated Hospital of Hubei Polytechnic University), Edong Healthcare Group, Huangshi, Hubei, China.
Abstract:
Inflammation and oxidative stress contribute to the initiation and progression of septic lung injury. MicroRNA-217 (miR-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 in vivo and mice were kept for 12 h to imitate septic lung injury. Next, mice were administrated with miR-217 antagomir or agomir to decrease or increase the expression of miR-217 in lung tissue. Moreover, primary peritoneal macrophages were separated and incubated with lipopolysaccharide (LPS) to further verify the role of miR-217 in vitro. miR-217 was upregulated in septic lungs and primary macrophages. miR-217 antagomir alleviated, whereas miR-217 agomir aggravated inflammation and oxidative stress in septic mice and LPS-stimulated macrophages. Further detection identified SIRT1 was responsible for miR-217 antagomir-mediated anti-inflammatory and anti-oxidant effects, and SIRT1 inhibition abolished the beneficial effects of miR-217 antagomir in vivo and in vitro. Our data defined miR-217 as a therapeutic target for treating septic lung injury.
Insights
MicroRNA-217 (miR-217) plays a key role in septic lung injury by regulating inflammation and oxidative stress. Targeting miR-217 offers a potential therapeutic strategy for this condition.
Area of Science:
- Molecular Biology
- Immunology
- Pathology
Background:
- Septic lung injury involves inflammation and oxidative stress.
- The specific role of microRNA-217 (miR-217) in septic lung injury pathogenesis is unclear.
- miR-217 is known to influence inflammatory and oxidative stress responses.
Purpose of the Study:
- To investigate the role and mechanism of miR-217 in septic lung injury.
- To determine if miR-217 can be a therapeutic target for septic lung injury.
Main Methods:
- Sepsis was induced in mice using caecal ligation and puncture.
- miR-217 expression was modulated using antagomirs and agomirs in vivo and in vitro.
- Primary peritoneal macrophages were stimulated with lipopolysaccharide (LPS) for in vitro studies.
- SIRT1's involvement was assessed through inhibition experiments.
Main Results:
- miR-217 expression was found to be upregulated in septic lungs and macrophages.
- Inhibiting miR-217 (antagomir) reduced inflammation and oxidative stress in sepsis models.
- Enhancing miR-217 (agomir) exacerbated inflammation and oxidative stress.
- SIRT1 mediated the anti-inflammatory and anti-oxidant effects of miR-217 inhibition.
Conclusions:
- miR-217 is upregulated during septic lung injury and contributes to its progression.
- Modulating miR-217 levels, particularly through inhibition, demonstrates therapeutic potential.
- The miR-217/SIRT1 axis is a critical pathway in septic lung injury, highlighting miR-217 as a therapeutic target.
