Registro completo |
Provedor de dados: |
BABT
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País: |
Brazil
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Título: |
A Mechanism Study of NMDAR1 in A Rat Alzheimer Disease (AD) Model
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Autores: |
Peng,Tianzhong
Huang,Xuedi
Hu,Suifa
Xie,Gui
Zhou,Cheng
Xiong,Jia
Liu,Rui
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Data: |
2017-01-01
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Ano: |
2017
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Palavras-chave: |
NMDAR1
Alzheimer disease
Aquaporin
AQP-1
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Resumo: |
ABSTRACT This study aimed to investigate the expression and mechanism of N- methyl -D- aspartate receptor 1 (NMDAR1) in the pathogenesis of Alzheimer disease (AD). Eighty adult Wistar rats were randomly divided into 4 groups (n=20 each) to receive an injection of 0, 5, 7 and 10 μl of 1 μg/μl amyloid-β 42 (Aβ1-42) in the hippocampus. Twenty rats in normal control group were injected with equal volume of saline. After 10 days, the hippocampus was isolated from 5 randomly selected rats in each group. The NMDAR1 protein and mRNA expression was determined by immunohistochemical staining and qRT-PCR. The aquaporin-1 (AQP-1) mRNA expression was also measured by qRT-PCR. We found that both NMDAR1 and AQP-1 expression in Aβ1-42 groups was increased in a dose-dependent manner. NMDAR1 and AQP-1 expression in 7 and 10 μl Aβ1-42 groups was significantly higher compared with 0 μl Aβ1-42 group (P <0.01). Further, the 10 μl Aβ1-42 group was randomly divided into 3 subgroups: AD-NMDA, AD-MK-801, and AD-Ctrl subgroup, which was given an intraperitoneal injection of NMDAR agonist NMDA, NMDAR antagonist MK-801 and saline, respectively. The relative APQ-1 expression in each subgroup was determined by qRT-PCR and Western blot analysis after 24 h. The AQP-1 expression was significantly decreased in AD-MK-801 group (P < 0.05), but was markedly increased in AD-NMDA group when compared with AD-Ctrl group (P <0.01). Our study suggested that expression abnormity of NMDAR1 is involved in the pathogenesis of AD. NMDAR1 might regulate the pathogenic process through stimulating the expression of AQP-1.
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Tipo: |
Info:eu-repo/semantics/article
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Idioma: |
Inglês
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Identificador: |
http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1516-89132017000100435
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Editor: |
Instituto de Tecnologia do Paraná - Tecpar
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Relação: |
10.1590/1678-4324-2017160481
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Formato: |
text/html
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Fonte: |
Brazilian Archives of Biology and Technology v.60 2017
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Direitos: |
info:eu-repo/semantics/openAccess
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