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

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-kappa B). 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-kappa B activity and phosphorylation of inhibitor of kappa B alpha (I kappa B alpha). Results NF-kappa B activation and LPS-induced histopathological changes in the lungs were significantly alleviated in the RIPC group. RIPC reduced phosphorylation of I kappa B alpha in lung tissue of ALI mice. Conclusions RIPC attenuates endotoxin-induced indirect ALI. This attenuation might occur through modification of NF-kappa B mediation of cytokines by modulating phosphorylation of I kappa B alpha.