NDLI: Gastrodin protects against LPS-induced acute lung injury by activating Nrf2 signaling pathway.

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Gastrodin protects against LPS-induced acute lung injury by activating Nrf2 signaling pathway.

Content Provider	Europe PMC
Author	Zhang, Zhuo Zhou, Jie Song, Daqiang Sun, Yuhong Liao, Changli Jiang, Xian
Copyright Year	2017
Abstract	Gastrodin (GAS), a phenolic glucoside derived from Gastrodiaelata Blume, has been reported to have anti-inflammatory effect. The aim of this study was to investigate the effects of GAS on LPS-induced acute lung injury in mice. ALI was induced by the intranasal administration of LPS and GAS was given 1 h or 12 h after LPS treatment. The results indicated that GAS treatment markedly attenuated the damage of lung injury induced by LPS. GAS attenuated the activity of myeloperoxidase (MPO) and down-regulated the levels of pro-inflammatory cytokines TNF-α, IL-6 and IL-1β in BALF. LPS-induced lung edema and lung function were also reversed by GAS. Furthermore, GAS was found to inhibit LPS-induced inflammatory cells infiltration. In addition, treatment of GAS inhibited LPS-induced NF-κB activation and up-regulated the expression of Nrf2 and HO-1. In conclusion, our results indicated that GAS had anti-inflammatory effects on LPS-induced acute lung injury. The anti-inflammatory mechanism of GAS was through the inhibition of NF-κB and activation of Nrf2 signaling pathways.
Journal	Oncotarget
Volume Number	8
PubMed Central reference number	PMC5458274
Issue Number	19
PubMed reference number	28389632
e-ISSN	19492553
DOI	10.18632/oncotarget.16740
Language	English
Publisher	Impact Journals LLC
Publisher Date	2017-05-01
Access Restriction	Open
Rights License	This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC-BY), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Copyright: © 2017 Zhang et al.
Subject Keyword	gastrodin LPS Nrf2 lung injury
Content Type	Text
Resource Type	Article
Subject	Oncology

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