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Exploration of Potential Molecular Targets of Dexmedetomidine in the Intestinal Repair of Burnt Rats
BACKGROUND: More and more burn survivors were suffering from varying degrees of damage to the intestinal barrier. Dexmedetomidine (Dex) was frequently used as sedative in more cases, but it was found to have repair effect on intestinal barrier dysfunction recently. This study aimed to explore the po...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove
2021
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8286122/ https://www.ncbi.nlm.nih.gov/pubmed/34285543 http://dx.doi.org/10.2147/JIR.S315952 |
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author | Qin, Chao Jiang, Yi Yu, Mingdong Bian, Yingxue Yu, Yonghao |
author_facet | Qin, Chao Jiang, Yi Yu, Mingdong Bian, Yingxue Yu, Yonghao |
author_sort | Qin, Chao |
collection | PubMed |
description | BACKGROUND: More and more burn survivors were suffering from varying degrees of damage to the intestinal barrier. Dexmedetomidine (Dex) was frequently used as sedative in more cases, but it was found to have repair effect on intestinal barrier dysfunction recently. This study aimed to explore the potential specific targets of Dex in intestinal barrier repair in burn rats model. METHODS: Male adult SD rats were used to establish 40% TBSA III degree scald model in our study. The samples were divided into four groups: burn rats (Burn), burn rats with Dex medication (Burn-Dex), sham rats (Sham) and sham rats with Dex medication (Sham-Dex). And plasma FITC-dextran and diamine oxidase (DAO) were detected to determine the intestinal permeability. Differentially expressed proteins were further adopted to protein–protein interaction network analysis, Gene Ontology analysis (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis. RESULTS: It showed that 40% TBSA III degree scald model was successfully constructed. And plasma FITC-dextran and DAO decreased significantly after Dex administration. Additionally, differentially expressed genes Psmb10, Psmb7 among the experimental groups were screened, which were significantly enriched in proteasome and other several pathways. CONCLUSION: The results above suggested that Q4KM35 and Q9JHW0, which are encoded by Psmb10 and Psmb7, respectively, are two possible protein targets of Dex in intestinal barrier repair. |
format | Online Article Text |
id | pubmed-8286122 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Dove |
record_format | MEDLINE/PubMed |
spelling | pubmed-82861222021-07-19 Exploration of Potential Molecular Targets of Dexmedetomidine in the Intestinal Repair of Burnt Rats Qin, Chao Jiang, Yi Yu, Mingdong Bian, Yingxue Yu, Yonghao J Inflamm Res Original Research BACKGROUND: More and more burn survivors were suffering from varying degrees of damage to the intestinal barrier. Dexmedetomidine (Dex) was frequently used as sedative in more cases, but it was found to have repair effect on intestinal barrier dysfunction recently. This study aimed to explore the potential specific targets of Dex in intestinal barrier repair in burn rats model. METHODS: Male adult SD rats were used to establish 40% TBSA III degree scald model in our study. The samples were divided into four groups: burn rats (Burn), burn rats with Dex medication (Burn-Dex), sham rats (Sham) and sham rats with Dex medication (Sham-Dex). And plasma FITC-dextran and diamine oxidase (DAO) were detected to determine the intestinal permeability. Differentially expressed proteins were further adopted to protein–protein interaction network analysis, Gene Ontology analysis (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis. RESULTS: It showed that 40% TBSA III degree scald model was successfully constructed. And plasma FITC-dextran and DAO decreased significantly after Dex administration. Additionally, differentially expressed genes Psmb10, Psmb7 among the experimental groups were screened, which were significantly enriched in proteasome and other several pathways. CONCLUSION: The results above suggested that Q4KM35 and Q9JHW0, which are encoded by Psmb10 and Psmb7, respectively, are two possible protein targets of Dex in intestinal barrier repair. Dove 2021-07-13 /pmc/articles/PMC8286122/ /pubmed/34285543 http://dx.doi.org/10.2147/JIR.S315952 Text en © 2021 Qin et al. https://creativecommons.org/licenses/by-nc/3.0/This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/ (https://creativecommons.org/licenses/by-nc/3.0/) ). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php). |
spellingShingle | Original Research Qin, Chao Jiang, Yi Yu, Mingdong Bian, Yingxue Yu, Yonghao Exploration of Potential Molecular Targets of Dexmedetomidine in the Intestinal Repair of Burnt Rats |
title | Exploration of Potential Molecular Targets of Dexmedetomidine in the Intestinal Repair of Burnt Rats |
title_full | Exploration of Potential Molecular Targets of Dexmedetomidine in the Intestinal Repair of Burnt Rats |
title_fullStr | Exploration of Potential Molecular Targets of Dexmedetomidine in the Intestinal Repair of Burnt Rats |
title_full_unstemmed | Exploration of Potential Molecular Targets of Dexmedetomidine in the Intestinal Repair of Burnt Rats |
title_short | Exploration of Potential Molecular Targets of Dexmedetomidine in the Intestinal Repair of Burnt Rats |
title_sort | exploration of potential molecular targets of dexmedetomidine in the intestinal repair of burnt rats |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8286122/ https://www.ncbi.nlm.nih.gov/pubmed/34285543 http://dx.doi.org/10.2147/JIR.S315952 |
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