Ischemic post-conditioning attenuates acute lung injury induced by intestinal ischemia–reperfusion in mice: role of Nrf2

Intestinal ischemic post-conditioning (IPo) protects against lung injury induced by intestinal ischemia–reperfusion (IIR) partly through promotion of expression and function of heme oxygenase-1 (HO-1). NF-E2-related factor-2 (Nrf2) is a key transcription factor that interacts with HO-1 and regulates...

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Bibliographic Details
Published in:Laboratory investigation 2016-10, Vol.96 (10), p.1087-1104
Main Authors: Meng, Qing-Tao, Cao, Chen, Wu, Yang, Liu, Hui-Min, Li, Wei, Sun, Qian, Chen, Rong, Xiao, Yong-Guang, Tang, Ling-Hua, Jiang, Ying, Leng, Yan, Lei, Shao-Qing, Lee, Chris C, Barry, Devin M, Chen, Xiangdong, Xia, Zhong-Yuan
Format: Article
Language:English
Subjects:
14/28
631/45/881
631/80/86/2366
64/60
96/95
Acute Lung Injury - etiology
Acute Lung Injury - metabolism
Acute Lung Injury - prevention & control
Animals
Glutathione Peroxidase - metabolism
Heme Oxygenase-1 - metabolism
Interleukin-6 - blood
Intestines - blood supply
Ischemic Postconditioning
Laboratory Medicine
Lung - enzymology
Male
Malondialdehyde - metabolism
Medicine
Medicine & Public Health
Membrane Proteins - metabolism
Mice, Inbred C57BL
NF-E2-Related Factor 2 - metabolism
Pathology
Random Allocation
Reperfusion Injury - complications
research-article
Superoxide Dismutase - metabolism
Tumor Necrosis Factor-alpha - blood
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Summary:Intestinal ischemic post-conditioning (IPo) protects against lung injury induced by intestinal ischemia–reperfusion (IIR) partly through promotion of expression and function of heme oxygenase-1 (HO-1). NF-E2-related factor-2 (Nrf2) is a key transcription factor that interacts with HO-1 and regulates antioxidant defense. However, the role of Nrf2 in IPo protection of IIR-induced pulmonary injury is not completely understood. Here we show that IPo significantly attenuated IIR-induced lung injury and suppressed oxidative stress and systemic inflammatory responses. IPo also increased the expression of both Nrf2 and HO-1. Consistently, the beneficial effects of IPo were abolished by ATRA and Brusatol, potent inhibitors of Nrf2. Moreover, the Nrf2 agonist t-BHQ showed similar activity as IPo. Taken together, our data suggest that Nrf2 activity, along with HO-1, plays an important role in the protective effects of IPo against IIR-induced acute lung injury.
ISSN:0023-6837
1530-0307
DOI:10.1038/labinvest.2016.87