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Hyperbaric oxygen therapy improves cognitive functioning after brain injury
Hyperbaric oxygen therapy has been widely applied and recognized in the treatment of brain injury; however, the correlation between the protective effect of hyperbaric oxygen therapy and changes of metabolites in the brain remains unclear. To investigate the effect and potential mechanism of hyperba...
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/PMC4145948/ https://www.ncbi.nlm.nih.gov/pubmed/25206655 http://dx.doi.org/10.3969/j.issn.1673-5374.2013.35.008 |
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author | Liu, Su Shen, Guangyu Deng, Shukun Wang, Xiubin Wu, Qinfeng Guo, Aisong |
author_facet | Liu, Su Shen, Guangyu Deng, Shukun Wang, Xiubin Wu, Qinfeng Guo, Aisong |
author_sort | Liu, Su |
collection | PubMed |
description | Hyperbaric oxygen therapy has been widely applied and recognized in the treatment of brain injury; however, the correlation between the protective effect of hyperbaric oxygen therapy and changes of metabolites in the brain remains unclear. To investigate the effect and potential mechanism of hyperbaric oxygen therapy on cognitive functioning in rats, we established traumatic brain injury models using Feeney's free falling method. We treated rat models with hyperbaric oxygen therapy at 0.2 MPa for 60 minutes per day. The Morris water maze test for spatial navigation showed that the average escape latency was significantly prolonged and cognitive function decreased in rats with brain injury. After treatment with hyperbaric oxygen therapy for 1 and 2 weeks, the rats’ spatial learning and memory abilities were improved. Hydrogen proton magnetic resonance spectroscopy analysis showed that the N-acetylaspartate/creatine ratio in the hippocampal CA3 region was significantly increased at 1 week, and the N-acetylaspartate/choline ratio was significantly increased at 2 weeks after hyperbaric oxygen therapy. Nissl staining and immunohistochemical staining showed that the number of nerve cells and Nissl bodies in the hippocampal CA3 region was significantly increased, and glial fibrillary acidic protein positive cells were decreased after a 2-week hyperbaric oxygen therapy treatment. Our findings indicate that hyperbaric oxygen therapy significantly improves cognitive functioning in rats with traumatic brain injury, and the potential mechanism is mediated by metabolic changes and nerve cell restoration in the hippocampal CA3 region. |
format | Online Article Text |
id | pubmed-4145948 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | Medknow Publications & Media Pvt Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-41459482014-09-09 Hyperbaric oxygen therapy improves cognitive functioning after brain injury Liu, Su Shen, Guangyu Deng, Shukun Wang, Xiubin Wu, Qinfeng Guo, Aisong Neural Regen Res Research and Report Article: Cognitive and Neural Regeneration Hyperbaric oxygen therapy has been widely applied and recognized in the treatment of brain injury; however, the correlation between the protective effect of hyperbaric oxygen therapy and changes of metabolites in the brain remains unclear. To investigate the effect and potential mechanism of hyperbaric oxygen therapy on cognitive functioning in rats, we established traumatic brain injury models using Feeney's free falling method. We treated rat models with hyperbaric oxygen therapy at 0.2 MPa for 60 minutes per day. The Morris water maze test for spatial navigation showed that the average escape latency was significantly prolonged and cognitive function decreased in rats with brain injury. After treatment with hyperbaric oxygen therapy for 1 and 2 weeks, the rats’ spatial learning and memory abilities were improved. Hydrogen proton magnetic resonance spectroscopy analysis showed that the N-acetylaspartate/creatine ratio in the hippocampal CA3 region was significantly increased at 1 week, and the N-acetylaspartate/choline ratio was significantly increased at 2 weeks after hyperbaric oxygen therapy. Nissl staining and immunohistochemical staining showed that the number of nerve cells and Nissl bodies in the hippocampal CA3 region was significantly increased, and glial fibrillary acidic protein positive cells were decreased after a 2-week hyperbaric oxygen therapy treatment. Our findings indicate that hyperbaric oxygen therapy significantly improves cognitive functioning in rats with traumatic brain injury, and the potential mechanism is mediated by metabolic changes and nerve cell restoration in the hippocampal CA3 region. Medknow Publications & Media Pvt Ltd 2013-12-15 /pmc/articles/PMC4145948/ /pubmed/25206655 http://dx.doi.org/10.3969/j.issn.1673-5374.2013.35.008 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: Cognitive and Neural Regeneration Liu, Su Shen, Guangyu Deng, Shukun Wang, Xiubin Wu, Qinfeng Guo, Aisong Hyperbaric oxygen therapy improves cognitive functioning after brain injury |
title | Hyperbaric oxygen therapy improves cognitive functioning after brain injury |
title_full | Hyperbaric oxygen therapy improves cognitive functioning after brain injury |
title_fullStr | Hyperbaric oxygen therapy improves cognitive functioning after brain injury |
title_full_unstemmed | Hyperbaric oxygen therapy improves cognitive functioning after brain injury |
title_short | Hyperbaric oxygen therapy improves cognitive functioning after brain injury |
title_sort | hyperbaric oxygen therapy improves cognitive functioning after brain injury |
topic | Research and Report Article: Cognitive and Neural Regeneration |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4145948/ https://www.ncbi.nlm.nih.gov/pubmed/25206655 http://dx.doi.org/10.3969/j.issn.1673-5374.2013.35.008 |
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