Pristimerin attenuates sepsis-induced lung injury by regulating nuclear factor kappaB/high-mobility group box 1 pathway

Purpose: To determine the effect of pristimerin on sepsis-induced lung injury, and the underlying mechanism of action. Methods: Lung injury was established in mice via induction of sepsis through cecal ligation and puncture (CLP). The effect of pristimerin was evaluated based on lung wet/dry weight and PaO2/FiO(2) ratios. Lung tissue was subjected to immunohistochemical and histopathological analyses, as well as Western blotting. Furthermore, the serum levels of inflammatory mediators were determined. Results: Pristimerin reversed the altered lung wet/dry weight ratio and PaO2/FiO(2) ratio in the lung, and also reduced lung injury score, relative to CLP group (p < 0.05). Moreover, it suppressed nucleocytoplasmic translocation of high mobility group protein B1 (HMGB1) in lung tissue. Serum levels of inflammatory mediators and expression levels of inducible nitric oxide synthase and nuclear factor-kappaB p65 were significantly reduced by pristimerin (p < 0.05). Conclusion: Pristimerin ameliorates sepsis-induced lung injury by inhibiting HMGB1/NF-kappa B. Thus, this compound has a potential for clinical application in the management of lung injury.