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Occludin and connexin 43 expression contribute to the pathogenesis of traumatic brain edema
The experimental model of traumatic brain injury was established in Sprague-Dawley rats according to Feeney's free falling method. The brains were harvested at 2, 6 and 24 hours, and at 3 and 5 days after injury. Changes in brain water content were determined using the wet and dry weights. Our...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Medknow Publications & Media Pvt Ltd
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4145997/ https://www.ncbi.nlm.nih.gov/pubmed/25206581 http://dx.doi.org/10.3969/j.issn.1673-5374.2013.29.002 |
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author | Ren, Wanyin Jing, Guojie Shen, Qin Yao, Xiaoteng Jing, Yingchao Lin, Feng Pan, Weidong |
author_facet | Ren, Wanyin Jing, Guojie Shen, Qin Yao, Xiaoteng Jing, Yingchao Lin, Feng Pan, Weidong |
author_sort | Ren, Wanyin |
collection | PubMed |
description | The experimental model of traumatic brain injury was established in Sprague-Dawley rats according to Feeney's free falling method. The brains were harvested at 2, 6 and 24 hours, and at 3 and 5 days after injury. Changes in brain water content were determined using the wet and dry weights. Our results showed that water content of tissue significantly increased after traumatic brain injury, and reached minimum at 24 hours. Hematoxylin-eosin staining revealed pathological impairment of brain tissue at each time point after injury, particularly at 3 days, with nerve cell edema, degenera-tion, and necrosis observed, and the apoptotic rate significantly increased. Immunohistochemistry and western blot analysis revealed that the expression of occludin at the injured site gradually de-creased as injury time advanced and reached a minimum at 3 days after injury; the expression of connexin 43 gradually increased as injury time advanced and reached a peak at 24 hours after in-jury. The experimental findings indicate that changes in occludin and connexin 43 expression were consistent with the development of brain edema, and may reflect the pathogenesis of brain injury. |
format | Online Article Text |
id | pubmed-4145997 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | Medknow Publications & Media Pvt Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-41459972014-09-09 Occludin and connexin 43 expression contribute to the pathogenesis of traumatic brain edema Ren, Wanyin Jing, Guojie Shen, Qin Yao, Xiaoteng Jing, Yingchao Lin, Feng Pan, Weidong Neural Regen Res Research and Report Article: Brain Injury and Neural Regeneration The experimental model of traumatic brain injury was established in Sprague-Dawley rats according to Feeney's free falling method. The brains were harvested at 2, 6 and 24 hours, and at 3 and 5 days after injury. Changes in brain water content were determined using the wet and dry weights. Our results showed that water content of tissue significantly increased after traumatic brain injury, and reached minimum at 24 hours. Hematoxylin-eosin staining revealed pathological impairment of brain tissue at each time point after injury, particularly at 3 days, with nerve cell edema, degenera-tion, and necrosis observed, and the apoptotic rate significantly increased. Immunohistochemistry and western blot analysis revealed that the expression of occludin at the injured site gradually de-creased as injury time advanced and reached a minimum at 3 days after injury; the expression of connexin 43 gradually increased as injury time advanced and reached a peak at 24 hours after in-jury. The experimental findings indicate that changes in occludin and connexin 43 expression were consistent with the development of brain edema, and may reflect the pathogenesis of brain injury. Medknow Publications & Media Pvt Ltd 2013-10-15 /pmc/articles/PMC4145997/ /pubmed/25206581 http://dx.doi.org/10.3969/j.issn.1673-5374.2013.29.002 Text en Copyright: © Neural Regeneration Research 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-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research and Report Article: Brain Injury and Neural Regeneration Ren, Wanyin Jing, Guojie Shen, Qin Yao, Xiaoteng Jing, Yingchao Lin, Feng Pan, Weidong Occludin and connexin 43 expression contribute to the pathogenesis of traumatic brain edema |
title | Occludin and connexin 43 expression contribute to the pathogenesis of traumatic brain edema |
title_full | Occludin and connexin 43 expression contribute to the pathogenesis of traumatic brain edema |
title_fullStr | Occludin and connexin 43 expression contribute to the pathogenesis of traumatic brain edema |
title_full_unstemmed | Occludin and connexin 43 expression contribute to the pathogenesis of traumatic brain edema |
title_short | Occludin and connexin 43 expression contribute to the pathogenesis of traumatic brain edema |
title_sort | occludin and connexin 43 expression contribute to the pathogenesis of traumatic brain edema |
topic | Research and Report Article: Brain Injury and Neural Regeneration |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4145997/ https://www.ncbi.nlm.nih.gov/pubmed/25206581 http://dx.doi.org/10.3969/j.issn.1673-5374.2013.29.002 |
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