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Systemic Administration of FC-77 Dampens Ischemia–Reperfusion-Induced Acute Lung Injury in Rats
Systemic administration of perfluorocarbons (PFCs) reportedly attenuates acute lung injury induced by acid aspiration and phorbol myristate acetate. However, the effects of PFCs on ischemia–reperfusion (IR)-induced lung injury have not been investigated. Typical acute lung injury was induced in rats...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer US
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7101555/ https://www.ncbi.nlm.nih.gov/pubmed/23807052 http://dx.doi.org/10.1007/s10753-013-9678-z |
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author | Chu, Shi-Jye Huang, Kun-Lun Wu, Shu-Yu Ko, Fu-Chang Wu, Geng-Chin Li, Rui-Ying Li, Min-Hui |
author_facet | Chu, Shi-Jye Huang, Kun-Lun Wu, Shu-Yu Ko, Fu-Chang Wu, Geng-Chin Li, Rui-Ying Li, Min-Hui |
author_sort | Chu, Shi-Jye |
collection | PubMed |
description | Systemic administration of perfluorocarbons (PFCs) reportedly attenuates acute lung injury induced by acid aspiration and phorbol myristate acetate. However, the effects of PFCs on ischemia–reperfusion (IR)-induced lung injury have not been investigated. Typical acute lung injury was induced in rats by 60 min of ischemia and 60 min of reperfusion in isolated and perfused rat lung model. Rat lungs were randomly assigned to receive PBS (control), 1 % FC-77, IR only, or IR with different doses of FC-77 (0.1 %, 0.5 %, or 1 %). Subsequently, bronchoalveolar lavage fluid (BALF), perfusate, and lung tissues were collected to evaluate the degree of lung injury. IR caused a significant increase in the following parameters: pulmonary arterial pressure, capillary filtration coefficient, lung weight gain, lung weight/body weight ratio, wet/dry lung weight ratio, and protein concentration in BALF. TNF-α and cytokine-induced neutrophil chemoattractant-1 concentrations in perfusate samples and MDA concentration and MPO activities in lung tissues were also significantly increased. Histopathology showed increased septal thickness and neutrophil infiltration in the lung tissues. Furthermore, NF-κB activity was significantly increased in the lungs. However, pretreatment with 1 % FC-77 prior to IR significantly attenuated the increases in these parameters. In conclusion, our results suggest that systemic FC-77 administration had a protective effect on IR-induced acute lung injury. These protective mechanisms may have been mediated by the inhibition of NF-κB activation and attenuation of subsequent inflammatory response. |
format | Online Article Text |
id | pubmed-7101555 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | Springer US |
record_format | MEDLINE/PubMed |
spelling | pubmed-71015552020-03-31 Systemic Administration of FC-77 Dampens Ischemia–Reperfusion-Induced Acute Lung Injury in Rats Chu, Shi-Jye Huang, Kun-Lun Wu, Shu-Yu Ko, Fu-Chang Wu, Geng-Chin Li, Rui-Ying Li, Min-Hui Inflammation Article Systemic administration of perfluorocarbons (PFCs) reportedly attenuates acute lung injury induced by acid aspiration and phorbol myristate acetate. However, the effects of PFCs on ischemia–reperfusion (IR)-induced lung injury have not been investigated. Typical acute lung injury was induced in rats by 60 min of ischemia and 60 min of reperfusion in isolated and perfused rat lung model. Rat lungs were randomly assigned to receive PBS (control), 1 % FC-77, IR only, or IR with different doses of FC-77 (0.1 %, 0.5 %, or 1 %). Subsequently, bronchoalveolar lavage fluid (BALF), perfusate, and lung tissues were collected to evaluate the degree of lung injury. IR caused a significant increase in the following parameters: pulmonary arterial pressure, capillary filtration coefficient, lung weight gain, lung weight/body weight ratio, wet/dry lung weight ratio, and protein concentration in BALF. TNF-α and cytokine-induced neutrophil chemoattractant-1 concentrations in perfusate samples and MDA concentration and MPO activities in lung tissues were also significantly increased. Histopathology showed increased septal thickness and neutrophil infiltration in the lung tissues. Furthermore, NF-κB activity was significantly increased in the lungs. However, pretreatment with 1 % FC-77 prior to IR significantly attenuated the increases in these parameters. In conclusion, our results suggest that systemic FC-77 administration had a protective effect on IR-induced acute lung injury. These protective mechanisms may have been mediated by the inhibition of NF-κB activation and attenuation of subsequent inflammatory response. Springer US 2013-06-27 2013 /pmc/articles/PMC7101555/ /pubmed/23807052 http://dx.doi.org/10.1007/s10753-013-9678-z Text en © Springer Science+Business Media New York 2013 This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic. |
spellingShingle | Article Chu, Shi-Jye Huang, Kun-Lun Wu, Shu-Yu Ko, Fu-Chang Wu, Geng-Chin Li, Rui-Ying Li, Min-Hui Systemic Administration of FC-77 Dampens Ischemia–Reperfusion-Induced Acute Lung Injury in Rats |
title | Systemic Administration of FC-77 Dampens Ischemia–Reperfusion-Induced Acute Lung Injury in Rats |
title_full | Systemic Administration of FC-77 Dampens Ischemia–Reperfusion-Induced Acute Lung Injury in Rats |
title_fullStr | Systemic Administration of FC-77 Dampens Ischemia–Reperfusion-Induced Acute Lung Injury in Rats |
title_full_unstemmed | Systemic Administration of FC-77 Dampens Ischemia–Reperfusion-Induced Acute Lung Injury in Rats |
title_short | Systemic Administration of FC-77 Dampens Ischemia–Reperfusion-Induced Acute Lung Injury in Rats |
title_sort | systemic administration of fc-77 dampens ischemia–reperfusion-induced acute lung injury in rats |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7101555/ https://www.ncbi.nlm.nih.gov/pubmed/23807052 http://dx.doi.org/10.1007/s10753-013-9678-z |
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