期刊
OXIDATIVE MEDICINE AND CELLULAR LONGEVITY
卷 2017, 期 -, 页码 -出版社
HINDAWI LTD
DOI: 10.1155/2017/9738745
关键词
-
类别
资金
- National Natural Science Foundation of China [31301171, 81601380]
- Natural Science Foundation of Anhui Province, China [1508085MH149]
- Colleges and Universities Provincial Young Talents Foundation Key Project [2013SQRL055ZD]
- Wannan Medical College Start Research Foundation Project [201223]
- Active Biological Macromolecules Research Provincial Key Laboratory Project [1306C083008]
- Natural Science Research Project of Anhui Colleges and Universities [KJ2016SD59]
- Colleges and Universities Outstanding Young Talent Support Programme Key Projects [gxyqZD2016173]
- Wuhu Technology Bureau Production and Research Cooperative Special Foundation [2013cxy04]
Myricitrin, a naturally occurring polyphenol hydroxy flavonoid, has been reported to possess anti-inflammatory properties. However, the precise molecular mechanism of myricitrin's effects on LPS-induced inflammation is unclear. In the present study, myricitrin significantly alleviated acute lung injury in mice. Myricitrin also markedly suppressed the production of NO, TNF-alpha, IL-6, and MCP-1 in RAW264.7 macrophage cells. The inhibition of NO was concomitant with a decrease in the protein and mRNA levels of iNOS. The phosphorylation of JAKs and STAT-1 was abrogated by myricitrin. Furthermore, myricitrin inhibited the nuclear transfer and DNA binding activity of STAT1. The JAK-specific inhibitor ruxolitinib simulated the anti-inflammatory effect of myricitrin. However, myricitrin had no impact on the MAPK signalling pathway. Myricitrin attenuated the generation of intracellular ROS by inhibiting the assembly of components of the gp91(phox) and p47(phox). Suppression of ROS generation using NAC or apocynin or by silencing gp91(phox) and p47(phox) all demonstrated that decreasing the level of ROS inhibited the LPS-induced inflammatory response. Collectively, these results confirmed that myricitrin exhibited anti-inflammatory activity by blocking the activation of JAKs and the downstream transcription factor STAT1, which may result from the downregulation of NOX2-dependent ROS production mediated by myricitrin.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据