Memory deficit associated with increased brain proinflammatory cytokine levels and neurodegeneration in acute ischemic stroke

被引:41
作者
Silva, Bruno [1 ]
Sousa, Larissa [1 ]
Miranda, Aline [2 ]
Vasconcelos, Anilton [1 ]
Reis, Helton [3 ]
Barcelos, Luciola [4 ]
Arantes, Rosa [1 ]
Teixeira, Antonio [2 ]
Rachid, Milene Alvarenga [1 ]
机构
[1] Univ Fed Minas Gerais, Inst Ciencias Biol, Dept Patol Geral, BR-31270901 Belo Horizonte, MG, Brazil
[2] Univ Fed Minas Gerais, Fac Med, Med Clin, BR-31270901 Belo Horizonte, MG, Brazil
[3] Univ Fed Minas Gerais, Inst Ciencias Biol, Dept Farmacol, BR-31270901 Belo Horizonte, MG, Brazil
[4] Univ Fed Minas Gerais, Inst Ciencias Biol Fisiol & Biofis, BR-31270901 Belo Horizonte, MG, Brazil
关键词
brain; ischemia; memory; inflammation; cytokines; CAROTID-ARTERY OCCLUSION; MICE; DAMAGE;
D O I
10.1590/0004-282X20150083
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The present study aimed to investigate behavioral changes and neuroinflammatory process following left unilateral common carotid artery occlusion (UCCA(O)), a model of cerebral ischemia. Post-ischemic behavioral changes following 15 min UCCA(O) were recorded 24 hours after reperfusion. The novel object recognition task was used to assess learning and memory. After behavioral test, brains from sham and ischemic mice were removed and processed to evaluate central nervous system pathology by TTC and H&E techniques as well as inflammatory mediators by ELISA. UCCA(O) promoted long-term memory impairment after reperfusion. Infarct areas were observed in the cerebrum by TTC stain. Moreover, the histopathological analysis revealed cerebral necrotic cavities surrounded by ischemic neurons and hippocampal neurodegeneration. In parallel with memory dysfunction, brain levels of TNF-a, IL-1b and CXCL1 were increased post ischemia compared with sham-operated group. These.ndings suggest an involvement of central nervous system inflammatory mediators and brain damage in cognitive impairment following unilateral acute ischemia.
引用
收藏
页码:655 / 659
页数:5
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