Data/hora: 06/06/2024 02:43:16

Provedor de dados: | 52
País: | Brazil
Título: | A Mechanism Study of NMDAR1 in A Rat Alzheimer Disease (AD) Model
Autores: | Peng,Tianzhong; Huang,Xuedi; Hu,Suifa; Xie,Gui; Zhou,Cheng; Xiong,Jia; Liu,Rui.
Data: | 2017-01-01
Ano: | 2017
Palavras-chave: | NMDAR1; Alzheimer disease; Aquaporin; AQP-1.
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 &lt;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 &lt; 0.05), but was markedly increased in AD-NMDA group when compared with AD-Ctrl group (P &lt;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.
Tipo: | Info:eu-repo/semantics/article
Idioma: | Inglês
Identificador: | http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1516-89132017000100435
Editor: | Instituto de Tecnologia do Paraná - Tecpar
Relação: | 10.1590/1678-4324-2017160481
Formato: | text/html
Fonte: | Brazilian Archives of Biology and Technology  v.60 2017
Fonte: | info:eu-repo/semantics/openAccess