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Time course changes of oxidative stress and inflammation in hyperoxia-induced acute lung injury in rats
OBJECTIVE(S): Therapies with high levels of oxygen are commonly used in the management of critical care. However, prolonged exposure to hyperoxia can cause acute lung injury. Although oxidative stress and inflammation are purported to play an important role in the pathogenesis of acute lung injury,...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Mashhad University of Medical Sciences
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4366750/ https://www.ncbi.nlm.nih.gov/pubmed/25810882 |
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author | Yu, Shouli Shi, Min Liu, Changting Liu, Qinghui Guo, Jun Yu, Senyang Jiang, Tingshu |
author_facet | Yu, Shouli Shi, Min Liu, Changting Liu, Qinghui Guo, Jun Yu, Senyang Jiang, Tingshu |
author_sort | Yu, Shouli |
collection | PubMed |
description | OBJECTIVE(S): Therapies with high levels of oxygen are commonly used in the management of critical care. However, prolonged exposure to hyperoxia can cause acute lung injury. Although oxidative stress and inflammation are purported to play an important role in the pathogenesis of acute lung injury, the exact mechanisms are still less known in the hyperoxic acute lung injury (HALI). MATERIALS AND METHODS: In this study, we investigated the time course changes of oxidative stress and inflammation in lung tissues of rats exposed to >95% oxygen for 12-60 hr. RESULTS: We found that at 12 hr after hyperoxia challenge, the activities of superoxide dismutase and glutathione peroxidase were significantly reduced with remarkably increased lipid peroxidation. At 12 hr, NF-κB p65 expression was also upregulated, but Iκ-Bα expression showed a remarkable decline. Significant production of inflammatory mediators, e.g, interleukin-1β, occurred 24 hr after hyperoxia exposure. In addition, the expression of intracellular adhesion molecule 1 expression and the activity of myeloperoxidase were significantly increased at 24 hr with a peak at 48 hr. CONCLUSION: Our data support that hyperoxia-induced oxidative damage and NF-κB pathway activation implicate in the early phase of HALI pathogenesis. |
format | Online Article Text |
id | pubmed-4366750 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Mashhad University of Medical Sciences |
record_format | MEDLINE/PubMed |
spelling | pubmed-43667502015-03-25 Time course changes of oxidative stress and inflammation in hyperoxia-induced acute lung injury in rats Yu, Shouli Shi, Min Liu, Changting Liu, Qinghui Guo, Jun Yu, Senyang Jiang, Tingshu Iran J Basic Med Sci Original Article OBJECTIVE(S): Therapies with high levels of oxygen are commonly used in the management of critical care. However, prolonged exposure to hyperoxia can cause acute lung injury. Although oxidative stress and inflammation are purported to play an important role in the pathogenesis of acute lung injury, the exact mechanisms are still less known in the hyperoxic acute lung injury (HALI). MATERIALS AND METHODS: In this study, we investigated the time course changes of oxidative stress and inflammation in lung tissues of rats exposed to >95% oxygen for 12-60 hr. RESULTS: We found that at 12 hr after hyperoxia challenge, the activities of superoxide dismutase and glutathione peroxidase were significantly reduced with remarkably increased lipid peroxidation. At 12 hr, NF-κB p65 expression was also upregulated, but Iκ-Bα expression showed a remarkable decline. Significant production of inflammatory mediators, e.g, interleukin-1β, occurred 24 hr after hyperoxia exposure. In addition, the expression of intracellular adhesion molecule 1 expression and the activity of myeloperoxidase were significantly increased at 24 hr with a peak at 48 hr. CONCLUSION: Our data support that hyperoxia-induced oxidative damage and NF-κB pathway activation implicate in the early phase of HALI pathogenesis. Mashhad University of Medical Sciences 2015-01 /pmc/articles/PMC4366750/ /pubmed/25810882 Text en Copyright: © Iranian Journal of Basic Medical Sciences http://creativecommons.org/licenses/by-nc-sa/3.0 This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Yu, Shouli Shi, Min Liu, Changting Liu, Qinghui Guo, Jun Yu, Senyang Jiang, Tingshu Time course changes of oxidative stress and inflammation in hyperoxia-induced acute lung injury in rats |
title | Time course changes of oxidative stress and inflammation in hyperoxia-induced acute lung injury in rats |
title_full | Time course changes of oxidative stress and inflammation in hyperoxia-induced acute lung injury in rats |
title_fullStr | Time course changes of oxidative stress and inflammation in hyperoxia-induced acute lung injury in rats |
title_full_unstemmed | Time course changes of oxidative stress and inflammation in hyperoxia-induced acute lung injury in rats |
title_short | Time course changes of oxidative stress and inflammation in hyperoxia-induced acute lung injury in rats |
title_sort | time course changes of oxidative stress and inflammation in hyperoxia-induced acute lung injury in rats |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4366750/ https://www.ncbi.nlm.nih.gov/pubmed/25810882 |
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