|本期目录/Table of Contents|

[1]段立晖,周国庆,孙芳,等.β-淀粉样蛋白对大鼠学习记忆、病理[J].医学研究与战创伤救治(原医学研究生学报),2009,11(05):389-393.
 DUAN Li-hui,ZHOU Guo-qing,SUN Fang,et al.The influence of beta-amyloid on learning and memory, histologic changes and tau hyperphosphorylation in rats[J].JOURNAL OF MEDICALRESEARCH —COMBAT TRAUMA CARE,2009,11(05):389-393.
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β-淀粉样蛋白对大鼠学习记忆、病理()

《医学研究与战创伤救治》(原医学研究生学报)[ISSN:1672-271X/CN:32-1713/R]

卷:
第11卷
期数:
2009年05期
页码:
389-393
栏目:
出版日期:
2009-09-20

文章信息/Info

Title:
The influence of beta-amyloid on learning and memory, histologic changes and tau hyperphosphorylation in rats
文章编号:
1672-271X(2009)05-0389-05
作者:
段立晖1周国庆1孙芳1夏树开2胡云龙2林世康2
1.南京军区南京总医院老年神经内科,江苏南京210002;2.南京川博生物科技有限公司,江苏南京210061
Author(s):
DUAN Li-hui1 ZHOU Guo-qing1 SUN Fang1XIA Shu-kai2 HU Yun-long2 LIN Shi-kang2
1. Department of Geriatric Neurology, Nanjing General Hospital of Nanjing Military Command, PLA, Nanjing 210002, Jiangsu, China; 2. Nanjing Chuanbo biotech Co., Ltd. Nanjing 210061, Jiangsu, China
关键词:
阿尔茨海默病动物模型大鼠β-淀粉样蛋白tau蛋白
Keywords:
Alzheimer’s disease Animal model Rat Beta-amyloid Tau protein
分类号:
R749.1
DOI:
-
文献标志码:
A
摘要:
目的研究大鼠海马区内注射β-淀粉样蛋白(Aβ)的神经毒性,建立阿尔茨海默病(AD)动物模型,探讨A β毒性机制。方法选取雌性成年SD大鼠24只,随机分为止常对照组、生 理盐水组、AD组,每组8只。Morris水迷宫检测大鼠学习记忆功能,HE染色及Bielschowski染色法观察海马神经元形态,免疫组化法观察tau蛋白异常磷酸化变化。结果与正常对照 组大鼠相比,AD组大鼠水迷富测试结果明显减退(P<0.01);海马CA1区神经元纤维形态紊乱,tau蛋白磷酸化阳性细胞数明显增多(P<0.01)。结论大鼠海马内注射凝集态A β可产生 神经毒性作用,能较好地模拟AD行为和病理表现,其神经毒性可能是通过tau蛋白的异常磷酸化起作用。
Abstract:
ObjectiveTo explore the neurotoxicity mechanism of beta-amyloid (Aβ) by establishment of Alzheimer’s disease model with injection Aβ to hippocampus in rats. Methods24 female rats were divided into three groups randomly: normal control group, saline group and AD group with each group 8 rats. The function of learning-memory was tested by Morris water maze. The pathological changes of hippocampus neurons were observed by both H-E staining and Bielschowski staining. The tau hyperphosphorylation was detected by immunohistochemistry staining. ResultsCompared with the normal control group rats, the function of learning-memory in AD group was impaired significantly (P<0.01), the neurofibrils in hippocampus neurons were disordered, and the number of P-tau positive cells was remarkably increased (P<0.01). ConclusionThe injection of aggregated Aβ25-35 to rat hippocampus can produce neurotoxicity, which mimics the performance of AD and pathological characterizations exactly. The tau hyperphosphorylation may be involved in the neurotoxic mechanisms of Aβ.

参考文献/References:

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备注/Memo

备注/Memo:
南京军区南京总医院科研基金资助项目(2006024)
更新日期/Last Update: 2013-11-20