Oncotarget

Research Papers:

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

Zhuo Zhang _, Jie Zhou, Daqiang Song, Yuhong Sun, Changli Liao and Xian Jiang

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Oncotarget. 2017; 8:32147-32156. https://doi.org/10.18632/oncotarget.16740

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Abstract

Zhuo Zhang1, Jie Zhou2, Daqiang Song1, Yuhong Sun1, Changli Liao3 and Xian Jiang4

1Laboratory of Pharmacology, College of Pharmacy, Southwest Medical University, Luzhou, Sichuan, China

2Laboratory of Science of Chinese Pharmacology, College of Pharmacy, Southwest Medical University, Luzhou, Sichuan, China

3Research Department, College of Pharmacy, Southwest Medical University, Luzhou, Sichuan, China

4Department of Anesthesiology, The Affiliated Hospital of College of Pharmacy, Southwest Medical University, Luzhou, Sichuan, China

Correspondence to:

Xian Jiang, email: jiangxian1716@163.com

Keywords: gastrodin, LPS, Nrf2, lung injury

Received: November 01, 2016    Accepted: February 10, 2017    Published: March 31, 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.


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