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

Zhuo Zhang; Jie Zhou; Daqiang Song; Yuhong Sun; Changli Liao; Xian Jiang

doi:10.18632/oncotarget.16740

Oncotarget

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

Its scope is unique. The term "oncotarget" encompasses all molecules, pathways, cellular functions, cell types, and even tissues that can be viewed as targets relevant to cancer as well as other diseases. The term was introduced in the inaugural Editorial, Introducing Oncotarget.

As of January 1, 2022, Oncotarget has shifted to a continuous publishing model. Papers will now be published continuously within yearly volumes in their final and complete form and then quickly released to Pubmed.

Subscribe to receive alerts once a paper has been published by Oncotarget.

Learn about our FREE

Post-Publication Promotion Services

50% on all publication fees until the end of 2024.

Impact Journals, LLC is the publisher of Oncotarget: www.impactjournals.com.

Impact Journals is a member of the Wellcome Trust List of Compliant Publishers.

Impact Journals is a member of the Society for Scholarly Publishing.

On December 23, 2022, Oncotarget server experienced a DDoS attack. As a result, Oncotarget site was inaccessible for a few hours. Oncotarget team swiftly dealt with the situation and took it under control. This malicious action will be reported to the FBI.

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

PDF | HTML | How to cite

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

Metrics: PDF 2147 views | HTML 3253 views | ?

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: [email protected]

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.

All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 16740

Publication Alerts

Post-Publication Promotion

Publication Discount

Research Papers:

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

Abstract