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 language | English |
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Pages (from-to) | 936-950 |
Number of pages | 15 |
Journal | Journal of International Medical Research |
Volume | 47 |
Issue number | 2 |
DOIs | |
Publication status | Published - 2019 Feb 1 |
Bibliographical note
Funding Information:This study was supported by the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Science, ICT, and Future Planning (No. NRF-2015R1A2A2A01006734).
Publisher Copyright:
© The Author(s) 2019.
Keywords
- Acute lung injury
- cytokine
- inflammation
- ischemic preconditioning
- mice
- survival rate
ASJC Scopus subject areas
- Biochemistry
- Cell Biology
- Biochemistry, medical