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Dexmedetomidine Protects Against Traumatic Brain Injury-Induced Acute Lung Injury in Mice

BACKGROUND: Traumatic brain injury (TBI) leads to acute lung injury (ALI), in which the inflammatory response plays an important role in its pathophysiology. Recent studies suggest that dexmedetomidine (Dex) plays a protective role in acute inflammatory diseases. However, whether Dex has a protectiv...

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Autores principales: Wang, Yuanyuan, Wang, Changli, Zhang, Dan, Wang, Huihui, Bo, Lulong, Deng, Xiaoming
Formato: Online Artículo Texto
Lenguaje:English
Publicado: International Scientific Literature, Inc. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6067036/
https://www.ncbi.nlm.nih.gov/pubmed/30013022
http://dx.doi.org/10.12659/MSM.908133
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author Wang, Yuanyuan
Wang, Changli
Zhang, Dan
Wang, Huihui
Bo, Lulong
Deng, Xiaoming
author_facet Wang, Yuanyuan
Wang, Changli
Zhang, Dan
Wang, Huihui
Bo, Lulong
Deng, Xiaoming
author_sort Wang, Yuanyuan
collection PubMed
description BACKGROUND: Traumatic brain injury (TBI) leads to acute lung injury (ALI), in which the inflammatory response plays an important role in its pathophysiology. Recent studies suggest that dexmedetomidine (Dex) plays a protective role in acute inflammatory diseases. However, whether Dex has a protective effect on TBI-induced ALI is not clear. The aim of this study was to investigate the effect of Dex on TBI-induced ALI in mice. MATERIAL/METHODS: Mice were randomly divided into 5 groups: 1) sham group; 2) TBI group; 3) TBI+Dex group; 4) TBI+atipamezole (Atip) group; and 5) TBI+Dex+Atip group. Dex (50 μg/kg) was intraperitoneal injected immediately after TBI. The α(2) adrenergic antagonist Atip (250 μg/kg) was intraperitoneal injected 15 minutes prior to Dex treatment. Then 24 hours later, the protein concentration in the bronchoalveolar lavage fluid (BALF), lung wet to dry weight ratio, hematoxylin and eosin (H&E) staining of lungs, the level of high-mobility group box protein 1(HMGB1) in serum, and the receptor for advanced glycation end products (RAGE) expression in lung were detected. RESULTS: Dex ameliorated the score of lung histological examination, as well as the severity of pulmonary edema and permeability. Moreover, Dex was observed to significantly suppress the expression of HMGBI and RAGE. However, the protective effects of Dex were partially reversed by the administration of Atip. CONCLUSIONS: Dex may protect against TBI-induced ALI via the HMGB1-RAGE signal pathway, and this protective effect is partly dependent on its α(2) adrenoceptor agonist action.
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spelling pubmed-60670362018-08-01 Dexmedetomidine Protects Against Traumatic Brain Injury-Induced Acute Lung Injury in Mice Wang, Yuanyuan Wang, Changli Zhang, Dan Wang, Huihui Bo, Lulong Deng, Xiaoming Med Sci Monit Animal Study BACKGROUND: Traumatic brain injury (TBI) leads to acute lung injury (ALI), in which the inflammatory response plays an important role in its pathophysiology. Recent studies suggest that dexmedetomidine (Dex) plays a protective role in acute inflammatory diseases. However, whether Dex has a protective effect on TBI-induced ALI is not clear. The aim of this study was to investigate the effect of Dex on TBI-induced ALI in mice. MATERIAL/METHODS: Mice were randomly divided into 5 groups: 1) sham group; 2) TBI group; 3) TBI+Dex group; 4) TBI+atipamezole (Atip) group; and 5) TBI+Dex+Atip group. Dex (50 μg/kg) was intraperitoneal injected immediately after TBI. The α(2) adrenergic antagonist Atip (250 μg/kg) was intraperitoneal injected 15 minutes prior to Dex treatment. Then 24 hours later, the protein concentration in the bronchoalveolar lavage fluid (BALF), lung wet to dry weight ratio, hematoxylin and eosin (H&E) staining of lungs, the level of high-mobility group box protein 1(HMGB1) in serum, and the receptor for advanced glycation end products (RAGE) expression in lung were detected. RESULTS: Dex ameliorated the score of lung histological examination, as well as the severity of pulmonary edema and permeability. Moreover, Dex was observed to significantly suppress the expression of HMGBI and RAGE. However, the protective effects of Dex were partially reversed by the administration of Atip. CONCLUSIONS: Dex may protect against TBI-induced ALI via the HMGB1-RAGE signal pathway, and this protective effect is partly dependent on its α(2) adrenoceptor agonist action. International Scientific Literature, Inc. 2018-07-17 /pmc/articles/PMC6067036/ /pubmed/30013022 http://dx.doi.org/10.12659/MSM.908133 Text en © Med Sci Monit, 2018 This work is licensed under Creative Common Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0 (https://creativecommons.org/licenses/by-nc-nd/4.0/) )
spellingShingle Animal Study
Wang, Yuanyuan
Wang, Changli
Zhang, Dan
Wang, Huihui
Bo, Lulong
Deng, Xiaoming
Dexmedetomidine Protects Against Traumatic Brain Injury-Induced Acute Lung Injury in Mice
title Dexmedetomidine Protects Against Traumatic Brain Injury-Induced Acute Lung Injury in Mice
title_full Dexmedetomidine Protects Against Traumatic Brain Injury-Induced Acute Lung Injury in Mice
title_fullStr Dexmedetomidine Protects Against Traumatic Brain Injury-Induced Acute Lung Injury in Mice
title_full_unstemmed Dexmedetomidine Protects Against Traumatic Brain Injury-Induced Acute Lung Injury in Mice
title_short Dexmedetomidine Protects Against Traumatic Brain Injury-Induced Acute Lung Injury in Mice
title_sort dexmedetomidine protects against traumatic brain injury-induced acute lung injury in mice
topic Animal Study
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6067036/
https://www.ncbi.nlm.nih.gov/pubmed/30013022
http://dx.doi.org/10.12659/MSM.908133
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