Maraviroc-Mediated Lung Protection following Trauma-Hemorrhagic Shock

Objectives. The peroxisome proliferator-activated receptor gamma (PPARγ) pathway exerts anti-inflammatory effects in response to injury. Maraviroc has been shown to have potent anti-inflammatory effects. The aim of this study was to investigate whether PPARγ plays an important role in maraviroc-med...

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Main Authors:	Liu, Fu-Chao, Zheng, Chih-Wen, Yu, Huang-Ping
Format:	Online
Language:	English
Published:	Hindawi Publishing Corporation 2016
Online Access:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4983395/

id	pubmed-4983395
recordtype	oai_dc
spelling	pubmed-49833952016-08-23 Maraviroc-Mediated Lung Protection following Trauma-Hemorrhagic Shock Liu, Fu-Chao Zheng, Chih-Wen Yu, Huang-Ping Research Article Objectives. The peroxisome proliferator-activated receptor gamma (PPARγ) pathway exerts anti-inflammatory effects in response to injury. Maraviroc has been shown to have potent anti-inflammatory effects. The aim of this study was to investigate whether PPARγ plays an important role in maraviroc-mediated lung protection following trauma-hemorrhage. Methods. Male Sprague-Dawley rats underwent trauma-hemorrhage (mean blood pressure maintained at approximately 35–40 mmHg for 90 minutes), followed by fluid resuscitation. During resuscitation, a single dose of maraviroc (3 mg/kg, intravenously) with and without a PPARγ inhibitor GW9662 (1 mg/kg, intravenously), GW9662, or vehicle was administered. Lung water content, tissue histology, and other various parameters were measured (n = 8 rats/group) 24 hours after resuscitation. One-way ANOVA and Tukey's testing were used for statistical analysis. Results. Trauma-hemorrhage significantly increased lung water content, myeloperoxidase activity, intercellular adhesion molecule-1, interleukin-6, and interleukin-1β levels. These parameters significantly improved in the maraviroc-treated rats subjected to trauma-hemorrhage. Maraviroc treatment also decreased lung tissue damage as compared to the vehicle-treated trauma-hemorrhaged rats. Coadministration of GW9662 with maraviroc abolished the maraviroc-induced beneficial effects on these parameters and lung injury. Conclusion. These results suggest that PPARγ might play a key role in maraviroc-mediated lung protection following trauma-hemorrhage. Hindawi Publishing Corporation 2016 2016-07-31 /pmc/articles/PMC4983395/ /pubmed/27556035 http://dx.doi.org/10.1155/2016/5302069 Text en Copyright © 2016 Fu-Chao Liu et al. https://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.
repository_type	Open Access Journal
institution_category	Foreign Institution
institution	US National Center for Biotechnology Information
building	NCBI PubMed
collection	Online Access
language	English
format	Online
author	Liu, Fu-Chao Zheng, Chih-Wen Yu, Huang-Ping
spellingShingle	Liu, Fu-Chao Zheng, Chih-Wen Yu, Huang-Ping Maraviroc-Mediated Lung Protection following Trauma-Hemorrhagic Shock
author_facet	Liu, Fu-Chao Zheng, Chih-Wen Yu, Huang-Ping
author_sort	Liu, Fu-Chao
title	Maraviroc-Mediated Lung Protection following Trauma-Hemorrhagic Shock
title_short	Maraviroc-Mediated Lung Protection following Trauma-Hemorrhagic Shock
title_full	Maraviroc-Mediated Lung Protection following Trauma-Hemorrhagic Shock
title_fullStr	Maraviroc-Mediated Lung Protection following Trauma-Hemorrhagic Shock
title_full_unstemmed	Maraviroc-Mediated Lung Protection following Trauma-Hemorrhagic Shock
title_sort	maraviroc-mediated lung protection following trauma-hemorrhagic shock
description	Objectives. The peroxisome proliferator-activated receptor gamma (PPARγ) pathway exerts anti-inflammatory effects in response to injury. Maraviroc has been shown to have potent anti-inflammatory effects. The aim of this study was to investigate whether PPARγ plays an important role in maraviroc-mediated lung protection following trauma-hemorrhage. Methods. Male Sprague-Dawley rats underwent trauma-hemorrhage (mean blood pressure maintained at approximately 35–40 mmHg for 90 minutes), followed by fluid resuscitation. During resuscitation, a single dose of maraviroc (3 mg/kg, intravenously) with and without a PPARγ inhibitor GW9662 (1 mg/kg, intravenously), GW9662, or vehicle was administered. Lung water content, tissue histology, and other various parameters were measured (n = 8 rats/group) 24 hours after resuscitation. One-way ANOVA and Tukey's testing were used for statistical analysis. Results. Trauma-hemorrhage significantly increased lung water content, myeloperoxidase activity, intercellular adhesion molecule-1, interleukin-6, and interleukin-1β levels. These parameters significantly improved in the maraviroc-treated rats subjected to trauma-hemorrhage. Maraviroc treatment also decreased lung tissue damage as compared to the vehicle-treated trauma-hemorrhaged rats. Coadministration of GW9662 with maraviroc abolished the maraviroc-induced beneficial effects on these parameters and lung injury. Conclusion. These results suggest that PPARγ might play a key role in maraviroc-mediated lung protection following trauma-hemorrhage.
publisher	Hindawi Publishing Corporation
publishDate	2016
url	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4983395/
_version_	1613627060777910272

Maraviroc-Mediated Lung Protection following Trauma-Hemorrhagic Shock

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