Neuroprotective effects of dexmedetomidine on traumatic brain injury: Involvement of neuronal apoptosis and HSP70 expression.
Mol Med Rep
; 17(6): 8079-8086, 2018 Jun.
Article
em En
| MEDLINE
| ID: mdl-29693126
ABSTRACT
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 SpragueDawley 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 weightdrop device and Dex (15 µg/kg) was intravenously administered immediately following TBI. The brain edema and neurological function outcomes of TBI were assessed using wetdry weight analysis and the Neurological Severity Score method. The expression levels of Bcell lymphoma2 (Bcl2) and Bcl2associated 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 postTBI improved brain edema and neurological outcomes, due to the attenuation of the TBIinduced reduction of Bax expression and increase of Bcl2 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.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Apoptose
/
Fármacos Neuroprotetores
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Proteínas de Choque Térmico HSP70
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Dexmedetomidina
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Lesões Encefálicas Traumáticas
Tipo de estudo:
Etiology_studies
/
Prognostic_studies
Limite:
Animals
Idioma:
En
Ano de publicação:
2018
Tipo de documento:
Article