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Ischemic Postconditioning Alleviates Intestinal Ischemia-Reperfusion Injury by Enhancing Autophagy and Suppressing Oxidative Stress through the Akt/GSK-3β/Nrf2 Pathway in Mice
AIMS: Ischemic postconditioning (IPO) has a strong protective effect against intestinal ischemia-reperfusion (IIR) injury that is partly related to autophagy. However, the precise mechanisms involved are unknown. METHODS: C57BL/6J mice were subjected to unilateral IIR with or without IPO. After 45 m...
Autores principales: | , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7102478/ https://www.ncbi.nlm.nih.gov/pubmed/32256957 http://dx.doi.org/10.1155/2020/6954764 |
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author | Chen, Rong Zhang, Yun-yan Lan, Jia-nan Liu, Hui-min Li, Wei Wu, Yang Leng, Yan Tang, Ling-hua Hou, Jia-bao Sun, Qian Sun, Tao Zeng, Zi Xia, Zhong-yuan Meng, Qing-tao |
author_facet | Chen, Rong Zhang, Yun-yan Lan, Jia-nan Liu, Hui-min Li, Wei Wu, Yang Leng, Yan Tang, Ling-hua Hou, Jia-bao Sun, Qian Sun, Tao Zeng, Zi Xia, Zhong-yuan Meng, Qing-tao |
author_sort | Chen, Rong |
collection | PubMed |
description | AIMS: Ischemic postconditioning (IPO) has a strong protective effect against intestinal ischemia-reperfusion (IIR) injury that is partly related to autophagy. However, the precise mechanisms involved are unknown. METHODS: C57BL/6J mice were subjected to unilateral IIR with or without IPO. After 45 min ischemia and 120 min reperfusion, intestinal tissues and blood were collected for examination. HE staining and Chiu's score were used to evaluate pathologic injury. We test markers of intestinal barrier function and oxidative stress. Finally, we used WB to detect the expression of key proteins of autophagy and the Akt/GSK-3β/Nrf2 pathway. RESULTS: IPO significantly attenuated IIR injury. Expression levels of LC3 II/I, Beclin-1, and p62 were altered during IIR, indicating that IPO enhanced autophagy. IPO also activated Akt, inhibited GSK-3β/Nrf2 pathway. CONCLUSION: Our study indicates that IPO can ameliorate IIR injury by evoking autophagy, activating Akt, inactivating GSK-3β, and activating Nrf2. These findings may provide novel insights for the alleviation of IIR injury.β/Nrf2 pathway. |
format | Online Article Text |
id | pubmed-7102478 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-71024782020-04-03 Ischemic Postconditioning Alleviates Intestinal Ischemia-Reperfusion Injury by Enhancing Autophagy and Suppressing Oxidative Stress through the Akt/GSK-3β/Nrf2 Pathway in Mice Chen, Rong Zhang, Yun-yan Lan, Jia-nan Liu, Hui-min Li, Wei Wu, Yang Leng, Yan Tang, Ling-hua Hou, Jia-bao Sun, Qian Sun, Tao Zeng, Zi Xia, Zhong-yuan Meng, Qing-tao Oxid Med Cell Longev Research Article AIMS: Ischemic postconditioning (IPO) has a strong protective effect against intestinal ischemia-reperfusion (IIR) injury that is partly related to autophagy. However, the precise mechanisms involved are unknown. METHODS: C57BL/6J mice were subjected to unilateral IIR with or without IPO. After 45 min ischemia and 120 min reperfusion, intestinal tissues and blood were collected for examination. HE staining and Chiu's score were used to evaluate pathologic injury. We test markers of intestinal barrier function and oxidative stress. Finally, we used WB to detect the expression of key proteins of autophagy and the Akt/GSK-3β/Nrf2 pathway. RESULTS: IPO significantly attenuated IIR injury. Expression levels of LC3 II/I, Beclin-1, and p62 were altered during IIR, indicating that IPO enhanced autophagy. IPO also activated Akt, inhibited GSK-3β/Nrf2 pathway. CONCLUSION: Our study indicates that IPO can ameliorate IIR injury by evoking autophagy, activating Akt, inactivating GSK-3β, and activating Nrf2. These findings may provide novel insights for the alleviation of IIR injury.β/Nrf2 pathway. Hindawi 2020-03-14 /pmc/articles/PMC7102478/ /pubmed/32256957 http://dx.doi.org/10.1155/2020/6954764 Text en Copyright © 2020 Rong Chen et al. http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Chen, Rong Zhang, Yun-yan Lan, Jia-nan Liu, Hui-min Li, Wei Wu, Yang Leng, Yan Tang, Ling-hua Hou, Jia-bao Sun, Qian Sun, Tao Zeng, Zi Xia, Zhong-yuan Meng, Qing-tao Ischemic Postconditioning Alleviates Intestinal Ischemia-Reperfusion Injury by Enhancing Autophagy and Suppressing Oxidative Stress through the Akt/GSK-3β/Nrf2 Pathway in Mice |
title | Ischemic Postconditioning Alleviates Intestinal Ischemia-Reperfusion Injury by Enhancing Autophagy and Suppressing Oxidative Stress through the Akt/GSK-3β/Nrf2 Pathway in Mice |
title_full | Ischemic Postconditioning Alleviates Intestinal Ischemia-Reperfusion Injury by Enhancing Autophagy and Suppressing Oxidative Stress through the Akt/GSK-3β/Nrf2 Pathway in Mice |
title_fullStr | Ischemic Postconditioning Alleviates Intestinal Ischemia-Reperfusion Injury by Enhancing Autophagy and Suppressing Oxidative Stress through the Akt/GSK-3β/Nrf2 Pathway in Mice |
title_full_unstemmed | Ischemic Postconditioning Alleviates Intestinal Ischemia-Reperfusion Injury by Enhancing Autophagy and Suppressing Oxidative Stress through the Akt/GSK-3β/Nrf2 Pathway in Mice |
title_short | Ischemic Postconditioning Alleviates Intestinal Ischemia-Reperfusion Injury by Enhancing Autophagy and Suppressing Oxidative Stress through the Akt/GSK-3β/Nrf2 Pathway in Mice |
title_sort | ischemic postconditioning alleviates intestinal ischemia-reperfusion injury by enhancing autophagy and suppressing oxidative stress through the akt/gsk-3β/nrf2 pathway in mice |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7102478/ https://www.ncbi.nlm.nih.gov/pubmed/32256957 http://dx.doi.org/10.1155/2020/6954764 |
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