Aim: Acute lung injury is a common clinical syndrome associated with significant morbidity. Myricetin has been demonstrated to inhibit inflammation in a variety of diseases. In this study, we aimed to investigate the protective effects of myricetin on inflammation in lipopolysaccharide-stimulated RAW 264.7 cells and lipopolysaccharide-induced lung injury model. Results/methodology: In this study, we detected the anti-inflammatory effects of myricetin by ELISA, RT-PCR and Western blot, respectively. Myricetin significantly inhibited the production of the proinflammatory cytokines in vitro and in vivo. It exerted an anti-inflammatory effect through suppressing the NF-κB p65 and AKT activation in NF-κB pathway and JNK, p-ERK and p38 in MAPK signaling pathway.
Conclusion: Myricetin alleviated acute lung injury by inhibiting macrophage activation, and inhibited inflammation in vitro and in vivo. It may be a potential therapeutic candidate for the prevention of inflammatory diseases.
Keywords: inflammatory diseases; lipopolysaccharide; macrophage; myricetin; acute lung injury.