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Biliverdin Protects the Isolated Rat Lungs from Ischemia-reperfusion Injury via Antioxidative, Anti-inflammatory and Anti-apoptotic Effects
BACKGROUND: Biliverdin (BV) has a protective role against ischemia-reperfusion injury (IRI). However, the protective role and potential mechanisms of BV on lung IRI (LIRI) remain to be elucidated. Thus, we aimed to investigate the protective role and potential mechanisms of BV on LIRI. METHODS: Lung...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Medknow Publications & Media Pvt Ltd
2017
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5381321/ https://www.ncbi.nlm.nih.gov/pubmed/28345551 http://dx.doi.org/10.4103/0366-6999.202735 |
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author | Tian, Wen-Fang Weng, Ping Sheng, Qiong Chen, Jun-Liang Zhang, Peng Zhang, Ji-Ru Du, Bin Wu, Min-Chen Pang, Qing-Feng Chu, Jian-Jun |
author_facet | Tian, Wen-Fang Weng, Ping Sheng, Qiong Chen, Jun-Liang Zhang, Peng Zhang, Ji-Ru Du, Bin Wu, Min-Chen Pang, Qing-Feng Chu, Jian-Jun |
author_sort | Tian, Wen-Fang |
collection | PubMed |
description | BACKGROUND: Biliverdin (BV) has a protective role against ischemia-reperfusion injury (IRI). However, the protective role and potential mechanisms of BV on lung IRI (LIRI) remain to be elucidated. Thus, we aimed to investigate the protective role and potential mechanisms of BV on LIRI. METHODS: Lungs were isolated from Sprague-Dawley rats to establish an ex vivo LIRI model. After an initial 15 min stabilization period, the isolated lungs were subjected to ischemia for 60 min, followed by 90 min of reperfusion with or without BV treatment. RESULTS: Lungs in the I/R group exhibited significant decrease in tidal volume (1.44 ± 0.23 ml/min in I/R group vs. 2.41 ± 0.31 ml/min in sham group; P < 0.001), lung compliance (0.27 ± 0.06 ml/cmH(2)O in I/R group vs. 0.44 ± 0.09 ml/cmH(2)O in sham group; P < 0.001; 1 cmH(2)O=0.098 kPa), and oxygen partial pressure (PaO(2)) levels (64.12 ± 12 mmHg in I/R group vs. 114 ± 8.0 mmHg in sham group; P < 0.001; 1 mmHg = 0.133 kPa). In contrast, these parameters in the BV group (2.27 ± 0.37 ml/min of tidal volume, 0.41 ± 0.10 ml/cmH(2)O of compliance, and 98.7 ± 9.7 mmHg of PaO(2)) were significantly higher compared with the I/R group (P = 0.004, P < 0.001, and P < 0.001, respectively). Compared to the I/R group, the contents of superoxide dismutase were significantly higher (47.07 ± 7.91 U/mg protein vs. 33.84 ± 10.15 U/mg protein; P = 0.005) while the wet/dry weight ratio (P < 0.01), methane dicarboxylic aldehyde (1.92 ± 0.25 nmol/mg protein vs. 2.67 ± 0.46 nmol/mg protein; P < 0.001), and adenosine triphosphate contents (297.05 ± 47.45 nmol/mg protein vs. 208.09 ± 29.11 nmol/mg protein; P = 0.005) were markedly lower in BV-treated lungs. Histological analysis revealed that BV alleviated LIRI. Furthermore, the expression of inflammatory cytokines (interleukin-1β, interleukin-6, and tumor necrosis factor-β) was downregulated and the expression of cyclooxygenase-2, inducible nitric oxide synthase, and Jun N-terminal kinase was significantly reduced in BV group (all P < 0.01 compared to I/R group). Finally, the apoptosis index in the BV group was significantly decreased (P < 0.01 compared to I/R group). CONCLUSION: BV protects lung IRI through its antioxidative, anti-inflammatory, and anti-apoptotic effects. |
format | Online Article Text |
id | pubmed-5381321 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Medknow Publications & Media Pvt Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-53813212017-04-26 Biliverdin Protects the Isolated Rat Lungs from Ischemia-reperfusion Injury via Antioxidative, Anti-inflammatory and Anti-apoptotic Effects Tian, Wen-Fang Weng, Ping Sheng, Qiong Chen, Jun-Liang Zhang, Peng Zhang, Ji-Ru Du, Bin Wu, Min-Chen Pang, Qing-Feng Chu, Jian-Jun Chin Med J (Engl) Original Article BACKGROUND: Biliverdin (BV) has a protective role against ischemia-reperfusion injury (IRI). However, the protective role and potential mechanisms of BV on lung IRI (LIRI) remain to be elucidated. Thus, we aimed to investigate the protective role and potential mechanisms of BV on LIRI. METHODS: Lungs were isolated from Sprague-Dawley rats to establish an ex vivo LIRI model. After an initial 15 min stabilization period, the isolated lungs were subjected to ischemia for 60 min, followed by 90 min of reperfusion with or without BV treatment. RESULTS: Lungs in the I/R group exhibited significant decrease in tidal volume (1.44 ± 0.23 ml/min in I/R group vs. 2.41 ± 0.31 ml/min in sham group; P < 0.001), lung compliance (0.27 ± 0.06 ml/cmH(2)O in I/R group vs. 0.44 ± 0.09 ml/cmH(2)O in sham group; P < 0.001; 1 cmH(2)O=0.098 kPa), and oxygen partial pressure (PaO(2)) levels (64.12 ± 12 mmHg in I/R group vs. 114 ± 8.0 mmHg in sham group; P < 0.001; 1 mmHg = 0.133 kPa). In contrast, these parameters in the BV group (2.27 ± 0.37 ml/min of tidal volume, 0.41 ± 0.10 ml/cmH(2)O of compliance, and 98.7 ± 9.7 mmHg of PaO(2)) were significantly higher compared with the I/R group (P = 0.004, P < 0.001, and P < 0.001, respectively). Compared to the I/R group, the contents of superoxide dismutase were significantly higher (47.07 ± 7.91 U/mg protein vs. 33.84 ± 10.15 U/mg protein; P = 0.005) while the wet/dry weight ratio (P < 0.01), methane dicarboxylic aldehyde (1.92 ± 0.25 nmol/mg protein vs. 2.67 ± 0.46 nmol/mg protein; P < 0.001), and adenosine triphosphate contents (297.05 ± 47.45 nmol/mg protein vs. 208.09 ± 29.11 nmol/mg protein; P = 0.005) were markedly lower in BV-treated lungs. Histological analysis revealed that BV alleviated LIRI. Furthermore, the expression of inflammatory cytokines (interleukin-1β, interleukin-6, and tumor necrosis factor-β) was downregulated and the expression of cyclooxygenase-2, inducible nitric oxide synthase, and Jun N-terminal kinase was significantly reduced in BV group (all P < 0.01 compared to I/R group). Finally, the apoptosis index in the BV group was significantly decreased (P < 0.01 compared to I/R group). CONCLUSION: BV protects lung IRI through its antioxidative, anti-inflammatory, and anti-apoptotic effects. Medknow Publications & Media Pvt Ltd 2017-04-05 /pmc/articles/PMC5381321/ /pubmed/28345551 http://dx.doi.org/10.4103/0366-6999.202735 Text en Copyright: © 2017 Chinese Medical Journal 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-ShareAlike 3.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms. |
spellingShingle | Original Article Tian, Wen-Fang Weng, Ping Sheng, Qiong Chen, Jun-Liang Zhang, Peng Zhang, Ji-Ru Du, Bin Wu, Min-Chen Pang, Qing-Feng Chu, Jian-Jun Biliverdin Protects the Isolated Rat Lungs from Ischemia-reperfusion Injury via Antioxidative, Anti-inflammatory and Anti-apoptotic Effects |
title | Biliverdin Protects the Isolated Rat Lungs from Ischemia-reperfusion Injury via Antioxidative, Anti-inflammatory and Anti-apoptotic Effects |
title_full | Biliverdin Protects the Isolated Rat Lungs from Ischemia-reperfusion Injury via Antioxidative, Anti-inflammatory and Anti-apoptotic Effects |
title_fullStr | Biliverdin Protects the Isolated Rat Lungs from Ischemia-reperfusion Injury via Antioxidative, Anti-inflammatory and Anti-apoptotic Effects |
title_full_unstemmed | Biliverdin Protects the Isolated Rat Lungs from Ischemia-reperfusion Injury via Antioxidative, Anti-inflammatory and Anti-apoptotic Effects |
title_short | Biliverdin Protects the Isolated Rat Lungs from Ischemia-reperfusion Injury via Antioxidative, Anti-inflammatory and Anti-apoptotic Effects |
title_sort | biliverdin protects the isolated rat lungs from ischemia-reperfusion injury via antioxidative, anti-inflammatory and anti-apoptotic effects |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5381321/ https://www.ncbi.nlm.nih.gov/pubmed/28345551 http://dx.doi.org/10.4103/0366-6999.202735 |
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