Aspectos clínicos, patológicos e inflamatórios durante a isquemia e reperfusão encefálica em camundongos

• Ano de defesa: 2017
• Autor(a) principal: Edna Constanza Gómez Victoria
• Tipo de documento: Tese
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Minas Gerais; UFMG
• Palavras-chave em Português: Cérebro; Isquemia; Acidente Vascular Cerebral; Citocinas; Camundongos; Receptores CCR5
• Link de acesso: http://hdl.handle.net/1843/FRSS-BBBGLV

In the present study, we used the BCCAo model for 25 minutes in wild C57BL/6 male mice to investigate neurological, pathological and inflammatory patterns during the acute phase from transient global ischemia in the brain. We observed neurological changes associated with morphological changes and inflammatory processes in the CNS, 72 hours after a reperfusion. Our results demonstrate brain levels of TNF, IL-1, CXCL1, and CCL5 were increased post-ischemia compared with sham-operated group. The activity of MPP-1 and MMP-2 was analyzed in the injury area by immunohistochemistry. The two markers increased in the BCCA group compared to the sham group. With the same BCCAo model in wild C57BL/6 and CCR5 receptor deficiente (CCR5-/-) C57BL/6 male mice, we investigate the involvement effects of CCR5 after ischemia. In CCR5 deficiency, we observed a significant improvement in the neurological deficits associated with the decrease of the infarcted area. In addition, a decrease in necrotic areas and ischemic neurons has been reported. C57BL/6 (CCR5-/-) ischemic mice showed lower levels of CXCL1 and higher levels of BDNF compared to C57BL/6 ischemic mice. Together, our results suggest potential neuroprotection in the absence of the CCR5 receptor in global ischemia/reperfusion injury. With the same BCCAo model. The present study demonstrated the association of neurological deficits with histopathological changes and expression of proinflammatory factors after cerebral ischemia and subacute eperfusion. Moreover, our data suggest a potential neuroprotection in the absence of the CCR5 receptor during global ischemia/reperfusion injury