Protective effect of quercetin on lipopolysaccharide-induced acute lung injury in mice by inhibiting inflammatory cell influx.

Sepsis may result in lung injury through a complex cascade of events including interstitium infiltration of inflammatory cells. Quercetin, the most abundant dietary flavonoid found in various plants and food products, possesses potent anti-inflammatory and antioxidative properties. The purpose of this study was to investigate whether preventive administration of quercetin could exert beneficial effects on experimental septic acute lung injury induced by lipopolysaccharide (LPS). C57/BL6 mice were challenged with LPS and survival time was monitored from 0-96 h after LPS treatment. Quercetin markedly rescued lethality, improved survival time, and inhibited serum necrosis factor a, interleukin 1 beta, and interleukin 6, and nitric oxide (NO), and increased IL-10 secretion. Moreover, quercetin decreased lung pathological changes, myeloperoxidase activity, and malondialdehyde levels. Quercetin also reduced the lung permeability changes and neutrophil and macrophage recruitment to the bronchoalveolar lavage fluid compared to the vehicle. Additionally, quercetin significantly reduced COX-2, HMGB1, iNOS expression, and NF-kappa B p65 phosphorylation. These results suggest that treatment with quercetin in septic mice improved survival time and lung injury. Quercetin may be a promising potential therapeutic reagent for LPS-induced acute lung injury.