›› 2009, Vol. 40 ›› Issue (2): 204-210.doi: 10.3969/j.issn.0529-1356.2009.02. 007

• 论著 • 上一篇    下一篇

晚期糖基化终产物受体和低密度脂蛋白受体相关蛋白在慢性脑血流低灌注大鼠皮层和海马的改变

刘宏1 ;邢安凤2 ;刘国贞1 ;李良1*   

  1. 1.首都医科大学基础医学院病理学教研室,北京 100069; 2.首都医科大学燕京医学院组织胚胎学教研室,北京 101300
  • 收稿日期:2008-06-02 修回日期:2008-07-30 出版日期:2009-04-06
  • 通讯作者: 李良

Changes of RAGE and LRP-1 in the cortex and hippocampus of rats with chronic cerebral hypoperfusion

  1. 1. Department of Pathology, College of Basic Medical Science, Capital Medical University, Beijing 100069, China; 2.Department of Histology and Embryology, Yanjing Medical College, Capital Medical University, Beijing 101300, China
  • Received:2008-06-02 Revised:2008-07-30 Online:2009-04-06
  • Contact: LI Liang

关键词: 晚期糖基化终产物受体, 低密度脂蛋白受体相关蛋白1, 慢性脑血流低灌注, β-淀粉样肽, 阿尔茨海默病, 免疫组织化学, 免疫印迹法, 大鼠

Abstract: Objective To investigate the change of receptor for advanced glycation and products(RAGE) and low-density lipoprotein receptor-related protein 1(LRP-1) in rats’ brain under the condition of chronic cerebral hypoperfusion. Methods Chronic cerebral blood hypoperfusion rat model made by bilateral common carotid artery permanent ligation was used, immunohistochemistry and Western blotting were employed to test the distribution and levels of RAGE and LRP-1 in cortex and hippocampus. Results Compared to controls, the immunoreactivity of RAGE was increased in microvascular endothelium from 10 days after hypoperfusion and decreased in neurons from 30 days after hypoperfusion in cortex and hippocampus, whereas the expression of LRP-1 was decreased in endothelium and increased in neurons. Western blotting results showed that levels of RAGE in cortex and hippocampus began to increase from 10 days after hypoperfusion significantly, while LRP-1 was significantly increased from 180 days after hypoperfusion. Conclusion Chronic cerebral hypoperfusion could lead to the changes of distribution of RAGE and LRP-1 between neuron and microvascular and increased expression of both protein, which implies that chronic cerebral hypoperfusion may play a very important role in early pathogenesis of Alzheimer’s disease (AD).

Key words: P>Receptor for advanced glycation end products, Low-density lipoprotein receptor-related protein 1, Chronic cerebral hypoperfusion, β-amyloid, Alzheimer’s disease, Immunohistochemistry, Western blotting, Rat/P>

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