Sevoflurane attenuates brain damage through inhibiting autophagy and apoptosis in cerebral ischemiareperfusion rats.
Mol Med Rep
; 21(1): 123-130, 2020 01.
Article
em En
| MEDLINE
| ID: mdl-31746402
ABSTRACT
The present study aimed to investigate the effects of sevoflurane postconditioning in a rat brain cerebral ischemiareperfusion (I/R) model and examine its possible mechanism. Rats were randomly divided into six groups Sham control group (Sham), I/R group, sevoflurane group (Se), Tolllike receptor4 (TLR4) inhibitor group (Tak242), nuclear factor (NF)κB inhibitor group (QNZ) and Sevoflurane postconditioning combined with TLR4NFκB signaling pathway inhibitor group (Se + Tak242). Morris water maze test and tetrazolium chloride staining were used to investigate the I/R injury. The nerve cell apoptosis and autophagy in cortical tissue were detected by TUNEL and transmission electron microscopy, respectively. The expression of TLR4 protein in cortical tissue was observed by immunohistochemical staining. The expression of autophagy and apoptotic associated proteins in cortical tissues and the activity of TLR4NFκB signaling pathway were assayed by western blot analysis. Sevoflurane postconditioning improved the learning and memory dysfunction caused by cerebral I/R injury. The cerebral infarction area, nerve cell apoptosis and formation of autophagic vacuoles were reduced after sevoflurane administration. The expression of light chain 3II/I, Beclin1, Bad and CleavedCaspase3 proteins were inhibited and the expression of Bcl2 protein was upregulated after sevoflurane administration. Sevoflurane postconditioning also inhibited the TLR4 protein and NFκB phosphorylation, and increased inhibitor of kBα phosphorylation. The treatment effect of Tak242 and QNZ groups were not significantly different compared with the Se group (P>0.05), and the Se + Tak242 group had the best results. The present study demonstrated that sevoflurane postconditioning could protect middle cerebral artery occlusioninduced brain injury rats by inhibiting autophagy and apoptosis, and that its mechanism is related to the TLR4NFκB signaling pathway.
Palavras-chave
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Traumatismo por Reperfusão
/
Transdução de Sinais
/
Córtex Cerebral
/
Apoptose
/
Sevoflurano
/
Neurônios
Idioma:
En
Ano de publicação:
2020
Tipo de documento:
Article