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Myricetin Attenuates LPS-induced Inflammation in RAW 264.7 Macrophages and Mouse Models

By Wei Hou, Siyi Hu, Zhenzhong Su, Qi Wang, Guangping Meng, Tingting Guo, Jie Zhang, Peng Gao

Posted 11 Apr 2018
bioRxiv DOI: 10.1101/299420 (published DOI: 10.4155/fmc-2018-0172)

Background: Myricetin has been demonstrated to inhibit inflammation in a variety of diseases, but little is known about its characters in acute lung injury (ALI). In this study, we aimed to investigate the protective effects of myricetin on inflammation in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells and a LPS-induced lung injury model. Methods: Specifically, we investigated its effects on lung edema and histological damage by lung W/D weight ratio, HE staining and Evans Blue dye. Then macrophage activation was detected by evaluating the TNF-α, IL-6 and IL-1β mRNA and protein iNOS and COX-2. Myricetin was used to detect the impact on the inflammatory responses in LPS-induced RAW264.7 cells with the same manners in mouse model. Finally, NF-κB and MAPK signaling pathways were investigated with Western blot assay in LPS-induced RAW264.7 cells. Results: Myricetin significantly inhibited the production of the pro-inflammatory cytokines in vitro and in vivo. The in vivo experiments showed that pretreatment with Myricetin markedly attenuated the development of pulmonary edema, histological severities and macrophage activation in mice with ALI. The underlying mechanisms were further demonstrated in vitro that myricetin 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 mitogen-activated protein kinases signaling pathway. Conclusion: Myricetin alleviated ALI 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.

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