Remote ischemic preconditioning ameliorates indirect acute lung injury by modulating phosphorylation of IκBα in mice

Yun-Hee Kim, Young Sung Kim, Byung Hwa Kim, Kuen Su Lee, Hyung Sun Park, Choon Hak Lim

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

Objective: Acute lung injury is responsible for mortality in seriously ill patients. Previous studies have shown that systemic inflammation is attenuated by remote ischemic preconditioning (RIPC) via reducing nuclear factor-kappa B (NF-κB). Therefore, we investigated whether lipopolysaccharide (LPS)-induced indirect acute lung injury (ALI) can be protected by RIPC. Methods: RIPC was accomplished by 10 minutes of occlusion using a tourniquet on the right hind limb of mice, followed by 10 minutes of reperfusion. This process was repeated three times. Intraperitoneal LPS (20 mg/kg) was administered to induce indirect ALI. Inflammatory cytokines in bronchoalveolar lavage fluid were analyzed using an enzyme-linked immunosorbent assay. Pulmonary tissue was excised for histological examination, and for examining NF-κB activity and phosphorylation of inhibitor of κBα (IκBα). Results: NF-κB activation and LPS-induced histopathological changes in the lungs were significantly alleviated in the RIPC group. RIPC reduced phosphorylation of IκBα in lung tissue of ALI mice. Conclusions: RIPC attenuates endotoxin-induced indirect ALI. This attenuation might occur through modification of NF-κB mediation of cytokines by modulating phosphorylation of IκBα.

Original languageEnglish
Pages (from-to)936-950
Number of pages15
JournalJournal of International Medical Research
Volume47
Issue number2
DOIs
Publication statusPublished - 2019 Feb 1

Keywords

  • Acute lung injury
  • cytokine
  • inflammation
  • ischemic preconditioning
  • mice
  • survival rate

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology
  • Biochemistry, medical

Fingerprint Dive into the research topics of 'Remote ischemic preconditioning ameliorates indirect acute lung injury by modulating phosphorylation of IκBα in mice'. Together they form a unique fingerprint.

  • Cite this