科研之友
微信
新浪微博
Facebook
分享链接
摘要
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 mu l of 1 mu g/mu l amyloid-beta 42 (A beta(1-42)) 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 A beta(1-42) groups was increased in a dose-dependent manner. NMDAR1 and AQP-1 expression in 7 and 10 mu l A beta(1-42) groups was significantly higher compared with 0 mu l A beta(1-42) group (P < 0.01). Further, the 10 mu l A beta(1-42) 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.
- 出版日期2017-12
- 单位江西中医药大学
