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J Stroke Cerebrovasc Dis ; 30(2): 105516, 2021 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-33310074

RESUMO

OBJECTIVE: To investigate the effects of different degrees of carotid artery stenosis (CAS) on the expression of XIAP and Smac in ischemic penumbra of rats with cerebral ischemia-reperfusion (I/R). MATERIALS AND METHODS: Samples were collected at 12 h and 24 h after reperfusion, and then the treated groups were divided into the NC-12 group, NC-24 group, MIS-12 group, MIS-24 group, MOS-12 group, MOS-24 group, SES-12 group and SES-24 group. HE staining was used to observe the pathological changes of the brain tissue. TUNEL assay was used to detect the apoptosis in the ischemic penumbra. IHC and RT-qPCR were used to detect the expression of XIAP and Smac in the brain tissue. RESULTS: By observing the pathological sections of brain tissue, the rats in MIS, MOS and SES groups showed loose brain tissue on the infarcted side and neuronal pyknosis in the ischemic penumbra. And with the aggravation and prolongation of the degree of stenosis, the degree of brain injury deepened. It was further found that the TUNEL positive rate was significantly increased in the ischemic penumbra in the SES and MOS groups compared with that in the normal control (NC) group. The results of IHC and RT-qPCR showed that the mRNA expression of XIAP and Smac in the ischemic penumbra was significantly up-regulated in the MIS, MOS and SES groups compared with that in the NC group. CONCLUSIONS: CAS may activate XIAP/Smac signaling pathway to induce neuronal apoptosis and promote the injury in the ischemic penumbra caused by cerebral I/R.


Assuntos
Proteínas Reguladoras de Apoptose/metabolismo , Isquemia Encefálica/etiologia , Encéfalo/metabolismo , Estenose das Carótidas/complicações , Proteínas Inibidoras de Apoptose/metabolismo , Proteínas Mitocondriais/metabolismo , Neurônios/metabolismo , Traumatismo por Reperfusão/etiologia , Animais , Apoptose , Proteínas Reguladoras de Apoptose/genética , Encéfalo/patologia , Isquemia Encefálica/patologia , Modelos Animais de Doenças , Proteínas Inibidoras de Apoptose/genética , Masculino , Proteínas Mitocondriais/genética , Neurônios/patologia , Ratos Sprague-Dawley , Traumatismo por Reperfusão/patologia , Índice de Gravidade de Doença , Transdução de Sinais , Fatores de Tempo
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