Myricitrin Modulates NADPH Oxidase-Dependent ROS Production to Inhibit Endotoxin-Mediated Inflammation by Blocking the JAKSTAT1 and NOX2p47phox Pathways
Joint Authors
Zhang, Yao
Qi, Shimei
Feng, Zunyong
Li, Qiang
Qi, Zhilin
Source
Oxidative Medicine and Cellular Longevity
Issue
Vol. 2017, Issue 2017 (31 Dec. 2017), pp.1-20, 20 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2017-06-20
Country of Publication
Egypt
No. of Pages
20
Main Subjects
Abstract EN
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-α, 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 gp91phox and p47phox.
Suppression of ROS generation using NAC or apocynin or by silencing gp91phox and p47phox 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.
American Psychological Association (APA)
Qi, Shimei& Feng, Zunyong& Li, Qiang& Qi, Zhilin& Zhang, Yao. 2017. Myricitrin Modulates NADPH Oxidase-Dependent ROS Production to Inhibit Endotoxin-Mediated Inflammation by Blocking the JAKSTAT1 and NOX2p47phox Pathways. Oxidative Medicine and Cellular Longevity،Vol. 2017, no. 2017, pp.1-20.
https://search.emarefa.net/detail/BIM-1196680
Modern Language Association (MLA)
Qi, Shimei…[et al.]. Myricitrin Modulates NADPH Oxidase-Dependent ROS Production to Inhibit Endotoxin-Mediated Inflammation by Blocking the JAKSTAT1 and NOX2p47phox Pathways. Oxidative Medicine and Cellular Longevity No. 2017 (2017), pp.1-20.
https://search.emarefa.net/detail/BIM-1196680
American Medical Association (AMA)
Qi, Shimei& Feng, Zunyong& Li, Qiang& Qi, Zhilin& Zhang, Yao. Myricitrin Modulates NADPH Oxidase-Dependent ROS Production to Inhibit Endotoxin-Mediated Inflammation by Blocking the JAKSTAT1 and NOX2p47phox Pathways. Oxidative Medicine and Cellular Longevity. 2017. Vol. 2017, no. 2017, pp.1-20.
https://search.emarefa.net/detail/BIM-1196680
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1196680