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Neuroprotective effects of mild hypothermia against traumatic brain injury by the involvement of the Nrf2/ARE pathway
BACKGROUND: Traumatic brain injury (TBI) is the leading cause of death and disability worldwide. Mild hypothermia (32–35°C) has been found to show neuroprotective effects against TBI. However, the specific mechanism is still elusive. In the current study, we explored the relationship between oxidati...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9392531/ https://www.ncbi.nlm.nih.gov/pubmed/35803901 http://dx.doi.org/10.1002/brb3.2686 |
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author | Yan, Chaolong Mao, Jiannan Yao, Chenbei Liu, Yang Yan, Huiying Jin, Wei |
author_facet | Yan, Chaolong Mao, Jiannan Yao, Chenbei Liu, Yang Yan, Huiying Jin, Wei |
author_sort | Yan, Chaolong |
collection | PubMed |
description | BACKGROUND: Traumatic brain injury (TBI) is the leading cause of death and disability worldwide. Mild hypothermia (32–35°C) has been found to show neuroprotective effects against TBI. However, the specific mechanism is still elusive. In the current study, we explored the relationship between oxidative damage after TBI and treatment with mild hypothermia as well as the underlying molecular mechanisms. METHODS: We used the closed cortex injury model to perform the brain injury and a temperature monitoring and control system to regulate the body temperature of mice after injury. Adult male C57BL/6 mice were adopted in this study and divided into four experimental groups. Tissue samples were harvested 24 h after injury. RESULTS: First, our results showed that treatment with mild hypothermia significantly improved neurobehavioral dysfunction and alleviated brain edema after TBI. Moreover, treatment with mild hypothermia enhanced the activity of the antioxidant enzymes superoxide dismutase and glutathione peroxidase and reduced the accumulation of lipid peroxidation malondialdehyde. Importantly, the expression and activation of the nuclear factor erythroid 2‐related factor 2‐antioxidant response element (Nrf2‐ARE) pathway were upregulated by mild hypothermia after TBI. Finally, treatment with hypothermia significantly decreased the cell apoptosis induced by TBI. CONCLUSION: Our results showed that the protective effects of mild hypothermia after TBI may be achieved by the upregulation of the Nrf2‐ARE pathway and revealed Nrf2 as a potentially important target to improve the prognosis of TBI. |
format | Online Article Text |
id | pubmed-9392531 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-93925312022-08-24 Neuroprotective effects of mild hypothermia against traumatic brain injury by the involvement of the Nrf2/ARE pathway Yan, Chaolong Mao, Jiannan Yao, Chenbei Liu, Yang Yan, Huiying Jin, Wei Brain Behav Original Articles BACKGROUND: Traumatic brain injury (TBI) is the leading cause of death and disability worldwide. Mild hypothermia (32–35°C) has been found to show neuroprotective effects against TBI. However, the specific mechanism is still elusive. In the current study, we explored the relationship between oxidative damage after TBI and treatment with mild hypothermia as well as the underlying molecular mechanisms. METHODS: We used the closed cortex injury model to perform the brain injury and a temperature monitoring and control system to regulate the body temperature of mice after injury. Adult male C57BL/6 mice were adopted in this study and divided into four experimental groups. Tissue samples were harvested 24 h after injury. RESULTS: First, our results showed that treatment with mild hypothermia significantly improved neurobehavioral dysfunction and alleviated brain edema after TBI. Moreover, treatment with mild hypothermia enhanced the activity of the antioxidant enzymes superoxide dismutase and glutathione peroxidase and reduced the accumulation of lipid peroxidation malondialdehyde. Importantly, the expression and activation of the nuclear factor erythroid 2‐related factor 2‐antioxidant response element (Nrf2‐ARE) pathway were upregulated by mild hypothermia after TBI. Finally, treatment with hypothermia significantly decreased the cell apoptosis induced by TBI. CONCLUSION: Our results showed that the protective effects of mild hypothermia after TBI may be achieved by the upregulation of the Nrf2‐ARE pathway and revealed Nrf2 as a potentially important target to improve the prognosis of TBI. John Wiley and Sons Inc. 2022-07-08 /pmc/articles/PMC9392531/ /pubmed/35803901 http://dx.doi.org/10.1002/brb3.2686 Text en © 2022 The Authors. Brain and Behavior published by Wiley Periodicals LLC. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Articles Yan, Chaolong Mao, Jiannan Yao, Chenbei Liu, Yang Yan, Huiying Jin, Wei Neuroprotective effects of mild hypothermia against traumatic brain injury by the involvement of the Nrf2/ARE pathway |
title | Neuroprotective effects of mild hypothermia against traumatic brain injury by the involvement of the Nrf2/ARE pathway |
title_full | Neuroprotective effects of mild hypothermia against traumatic brain injury by the involvement of the Nrf2/ARE pathway |
title_fullStr | Neuroprotective effects of mild hypothermia against traumatic brain injury by the involvement of the Nrf2/ARE pathway |
title_full_unstemmed | Neuroprotective effects of mild hypothermia against traumatic brain injury by the involvement of the Nrf2/ARE pathway |
title_short | Neuroprotective effects of mild hypothermia against traumatic brain injury by the involvement of the Nrf2/ARE pathway |
title_sort | neuroprotective effects of mild hypothermia against traumatic brain injury by the involvement of the nrf2/are pathway |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9392531/ https://www.ncbi.nlm.nih.gov/pubmed/35803901 http://dx.doi.org/10.1002/brb3.2686 |
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