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In vivo study of the effects of exogenous hydrogen sulfide on lung mitochondria in acute lung injury in rats
BACKGROUND: Acute lung injury (ALI) is a serious disease with high incidence in ICU, and impaired mitochondria function plays a significant role in ALI. In this study, we examined the possible roles of exogenous hydrogen sulfide (H(2)S) in lung mitochondria regulation in ALI rats. METHODS: The rat A...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4279795/ https://www.ncbi.nlm.nih.gov/pubmed/25550681 http://dx.doi.org/10.1186/1471-2253-14-117 |
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author | Du, Quansheng Wang, Chao Zhang, Nan Li, Guofeng Zhang, Meng Li, Liping Zhang, Qingzeng Zhang, Jianxin |
author_facet | Du, Quansheng Wang, Chao Zhang, Nan Li, Guofeng Zhang, Meng Li, Liping Zhang, Qingzeng Zhang, Jianxin |
author_sort | Du, Quansheng |
collection | PubMed |
description | BACKGROUND: Acute lung injury (ALI) is a serious disease with high incidence in ICU, and impaired mitochondria function plays a significant role in ALI. In this study, we examined the possible roles of exogenous hydrogen sulfide (H(2)S) in lung mitochondria regulation in ALI rats. METHODS: The rat ALI model was induced by an intra-tongue vein Lipopolysaccharide (LPS) injection. We used sodium hydrosulphide (NaHS) as the H(2)S donor. We randomly divided 40 Sprague–Dawley rats into five groups: control, LPS injury, LPS + low-dose NaHS (0.78 mg•kg(-1)), LPS + middle-dose NaHS (1.56 mg•kg(-1)), and LPS + high-dose NaHS (3.12 mg•kg(-1)). Rats were killed 3 h after NaHS administration. We calculated a semi-quantitative histological index of lung injury assessments and measured the lung wet-to-dry weight ratio. We further analyzed serum for interleukin-1β levels using enzyme-linked immunosorbent assays. We observed lung mitochondria ultrastructures with an electron microscope. We examined oxidative stress markers in lung mitochondria and the mitochondrial swelling and activity. We analyzed lung mitochondria and cytosol Cyt-c protein expression using Western blotting. RESULTS: Compared to the control group, the quantitative assessment score index, wet-to-dry weight ratios, and interleukin-1β content in the LPS injury group were significantly increased and the mitochondrial ultrastructure damaged. Furthermore, mitochondrial activity, adenosine triphosphatease, superoxide dismutase, glutathione peroxidase, and mitochondrial Cyt-c protein expression were significantly decreased, and malondialdehyde content, mitochondrial swelling, and cytosol Cyt-c protein expression were significantly increased in the LPS injury group compared to the control group. These effects were lessened by NaHS. CONCLUSION: Exogenous H(2)S provided a protective effect against ALI by decreasing the mitochondrial lipid peroxidation level and protecting the cell structure in the LPS-induced rat models. Its regulatory effect on lung mitochondria is positively correlated with the dosage. |
format | Online Article Text |
id | pubmed-4279795 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-42797952014-12-31 In vivo study of the effects of exogenous hydrogen sulfide on lung mitochondria in acute lung injury in rats Du, Quansheng Wang, Chao Zhang, Nan Li, Guofeng Zhang, Meng Li, Liping Zhang, Qingzeng Zhang, Jianxin BMC Anesthesiol Research Article BACKGROUND: Acute lung injury (ALI) is a serious disease with high incidence in ICU, and impaired mitochondria function plays a significant role in ALI. In this study, we examined the possible roles of exogenous hydrogen sulfide (H(2)S) in lung mitochondria regulation in ALI rats. METHODS: The rat ALI model was induced by an intra-tongue vein Lipopolysaccharide (LPS) injection. We used sodium hydrosulphide (NaHS) as the H(2)S donor. We randomly divided 40 Sprague–Dawley rats into five groups: control, LPS injury, LPS + low-dose NaHS (0.78 mg•kg(-1)), LPS + middle-dose NaHS (1.56 mg•kg(-1)), and LPS + high-dose NaHS (3.12 mg•kg(-1)). Rats were killed 3 h after NaHS administration. We calculated a semi-quantitative histological index of lung injury assessments and measured the lung wet-to-dry weight ratio. We further analyzed serum for interleukin-1β levels using enzyme-linked immunosorbent assays. We observed lung mitochondria ultrastructures with an electron microscope. We examined oxidative stress markers in lung mitochondria and the mitochondrial swelling and activity. We analyzed lung mitochondria and cytosol Cyt-c protein expression using Western blotting. RESULTS: Compared to the control group, the quantitative assessment score index, wet-to-dry weight ratios, and interleukin-1β content in the LPS injury group were significantly increased and the mitochondrial ultrastructure damaged. Furthermore, mitochondrial activity, adenosine triphosphatease, superoxide dismutase, glutathione peroxidase, and mitochondrial Cyt-c protein expression were significantly decreased, and malondialdehyde content, mitochondrial swelling, and cytosol Cyt-c protein expression were significantly increased in the LPS injury group compared to the control group. These effects were lessened by NaHS. CONCLUSION: Exogenous H(2)S provided a protective effect against ALI by decreasing the mitochondrial lipid peroxidation level and protecting the cell structure in the LPS-induced rat models. Its regulatory effect on lung mitochondria is positively correlated with the dosage. BioMed Central 2014-12-15 /pmc/articles/PMC4279795/ /pubmed/25550681 http://dx.doi.org/10.1186/1471-2253-14-117 Text en © Du et al.; licensee BioMed Central. 2014 This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Article Du, Quansheng Wang, Chao Zhang, Nan Li, Guofeng Zhang, Meng Li, Liping Zhang, Qingzeng Zhang, Jianxin In vivo study of the effects of exogenous hydrogen sulfide on lung mitochondria in acute lung injury in rats |
title | In vivo study of the effects of exogenous hydrogen sulfide on lung mitochondria in acute lung injury in rats |
title_full | In vivo study of the effects of exogenous hydrogen sulfide on lung mitochondria in acute lung injury in rats |
title_fullStr | In vivo study of the effects of exogenous hydrogen sulfide on lung mitochondria in acute lung injury in rats |
title_full_unstemmed | In vivo study of the effects of exogenous hydrogen sulfide on lung mitochondria in acute lung injury in rats |
title_short | In vivo study of the effects of exogenous hydrogen sulfide on lung mitochondria in acute lung injury in rats |
title_sort | in vivo study of the effects of exogenous hydrogen sulfide on lung mitochondria in acute lung injury in rats |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4279795/ https://www.ncbi.nlm.nih.gov/pubmed/25550681 http://dx.doi.org/10.1186/1471-2253-14-117 |
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