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Neuroprotective effects of dexmedetomidine on traumatic brain injury: Involvement of neuronal apoptosis and HSP70 expression

The aim of the present study was to investigate the protective effect of dexmedetomidine (Dex) on traumatic brain injury (TBI), and further evaluate whether the underlying neuroprotective mechanisms are associated with neurological apoptosis and the expression of 70 kDa heat shock protein (HSP70) in...

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Autores principales: Zhang, Man-He, Zhou, Xiu-Min, Cui, Jian-Zhong, Wang, Kai-Jie, Feng, Yan, Zhang, Hong-Ao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5983975/
https://www.ncbi.nlm.nih.gov/pubmed/29693126
http://dx.doi.org/10.3892/mmr.2018.8898
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author Zhang, Man-He
Zhou, Xiu-Min
Cui, Jian-Zhong
Wang, Kai-Jie
Feng, Yan
Zhang, Hong-Ao
author_facet Zhang, Man-He
Zhou, Xiu-Min
Cui, Jian-Zhong
Wang, Kai-Jie
Feng, Yan
Zhang, Hong-Ao
author_sort Zhang, Man-He
collection PubMed
description The aim of the present study was to investigate the protective effect of dexmedetomidine (Dex) on traumatic brain injury (TBI), and further evaluate whether the underlying neuroprotective mechanisms are associated with neurological apoptosis and the expression of 70 kDa heat shock protein (HSP70) in the hippocampus. A total of 90 adult male Sprague-Dawley rats were randomly assigned into 3 groups (n=30/group): Sham, TBI and Dex groups. The rat models of TBI were established using a modified weight-drop device and Dex (15 µg/kg) was intravenously administered immediately following TBI. The brain edema and neurological function outcomes of TBI were assessed using wet-dry weight analysis and the Neurological Severity Score method. The expression levels of B-cell lymphoma-2 (Bcl-2) and Bcl-2-associated X protein (Bax) in the rat hippocampus were evaluated using immunohistochemical staining and western blot analysis. The protein levels of HSP70 in the hippocampal region were analyzed using western blot analysis. The results of the present study revealed that administration of Dex post-TBI improved brain edema and neurological outcomes, due to the attenuation of the TBI-induced reduction of Bax expression and increase of Bcl-2 and HSP70 expression. In conclusion, the results of the present study suggested that administration of Dex may serve as a neuroprotective agent against brain injury, at least partially via the inhibition of neuronal apoptosis and upregulation of HSP70 expression in the hippocampus.
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spelling pubmed-59839752018-06-04 Neuroprotective effects of dexmedetomidine on traumatic brain injury: Involvement of neuronal apoptosis and HSP70 expression Zhang, Man-He Zhou, Xiu-Min Cui, Jian-Zhong Wang, Kai-Jie Feng, Yan Zhang, Hong-Ao Mol Med Rep Articles The aim of the present study was to investigate the protective effect of dexmedetomidine (Dex) on traumatic brain injury (TBI), and further evaluate whether the underlying neuroprotective mechanisms are associated with neurological apoptosis and the expression of 70 kDa heat shock protein (HSP70) in the hippocampus. A total of 90 adult male Sprague-Dawley rats were randomly assigned into 3 groups (n=30/group): Sham, TBI and Dex groups. The rat models of TBI were established using a modified weight-drop device and Dex (15 µg/kg) was intravenously administered immediately following TBI. The brain edema and neurological function outcomes of TBI were assessed using wet-dry weight analysis and the Neurological Severity Score method. The expression levels of B-cell lymphoma-2 (Bcl-2) and Bcl-2-associated X protein (Bax) in the rat hippocampus were evaluated using immunohistochemical staining and western blot analysis. The protein levels of HSP70 in the hippocampal region were analyzed using western blot analysis. The results of the present study revealed that administration of Dex post-TBI improved brain edema and neurological outcomes, due to the attenuation of the TBI-induced reduction of Bax expression and increase of Bcl-2 and HSP70 expression. In conclusion, the results of the present study suggested that administration of Dex may serve as a neuroprotective agent against brain injury, at least partially via the inhibition of neuronal apoptosis and upregulation of HSP70 expression in the hippocampus. D.A. Spandidos 2018-06 2018-04-19 /pmc/articles/PMC5983975/ /pubmed/29693126 http://dx.doi.org/10.3892/mmr.2018.8898 Text en Copyright: © Zhang et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Zhang, Man-He
Zhou, Xiu-Min
Cui, Jian-Zhong
Wang, Kai-Jie
Feng, Yan
Zhang, Hong-Ao
Neuroprotective effects of dexmedetomidine on traumatic brain injury: Involvement of neuronal apoptosis and HSP70 expression
title Neuroprotective effects of dexmedetomidine on traumatic brain injury: Involvement of neuronal apoptosis and HSP70 expression
title_full Neuroprotective effects of dexmedetomidine on traumatic brain injury: Involvement of neuronal apoptosis and HSP70 expression
title_fullStr Neuroprotective effects of dexmedetomidine on traumatic brain injury: Involvement of neuronal apoptosis and HSP70 expression
title_full_unstemmed Neuroprotective effects of dexmedetomidine on traumatic brain injury: Involvement of neuronal apoptosis and HSP70 expression
title_short Neuroprotective effects of dexmedetomidine on traumatic brain injury: Involvement of neuronal apoptosis and HSP70 expression
title_sort neuroprotective effects of dexmedetomidine on traumatic brain injury: involvement of neuronal apoptosis and hsp70 expression
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5983975/
https://www.ncbi.nlm.nih.gov/pubmed/29693126
http://dx.doi.org/10.3892/mmr.2018.8898
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