β-Asarone Mitigates Amyloidosis and Downregulates RAGE in a Transgenic Mouse Model of Alzheimer’s Disease

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• 作者：Cong Yang ; Xiaoguang Li ; Yousheng Mo ; Sijun Liu…
• 关键词：Alzheimer’s disease ; β ; Asarone ; Aβ plaques ; Aβ1 ; 42 ; Advanced glycation end products
• 刊名：Cellular and Molecular Neurobiology
• 出版年：2016
• 出版时间：January 2016
• 年：2016
• 卷：36
• 期：1
• 页码：121-130
• 全文大小：2,412 KB
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• 作者单位：Cong Yang (1)
  Xiaoguang Li (1)
  Yousheng Mo (1)
  Sijun Liu (1)
  Luguang Zhao (1)
  Xiaohui Ma (1)
  Zhigang Fang (1)
  Junli Chen (1)
  Yunbo Chen (1)
  Xuhua Yu (1)
  Shuhuan Fang (1)
  Yongbin Zhang (2)
  Shaoxiang Xian (3)
  Qi Wang (1)
  
  1. Institute of Clinical Pharmacology, Guangzhou University of Chinese Medicine, Guangzhou, 510405, China
  2. Laboratory of Experimental Animal, Guangzhou University of Chinese Medicine, Guangzhou, 510405, China
  3. Chinese Internal Medicine, Guangzhou University of Chinese Medicine, Guangzhou, 510405, China
  
• 刊物类别：Biomedical and Life Sciences
• 刊物主题：Biomedicine
  Neurosciences
  Animal Anatomy, Morphology and Histology
  
• 出版者：Springer Netherlands
• ISSN：1573-6830

文摘

Elevated β-amyloid (Aβ) is a hallmark of Alzheimer’s disease (AD). Recent evidence has suggested that the receptor of advanced glycation end products (RAGE) is a key target for Aβ-induced perturbation in AD, and blockade of RAGE significantly alleviates synaptic injury. Our previous study has suggested that β-asarone could reduce neuronal apoptosis and improve memory deficits in β-amyloid precursor protein and presenilin-1 (APP/PS1) double transgenic AD-model mice. In the present study, we evaluated the effects of β-asarone on amyloidosis in APP/PS1 mice. We found that the survival of neurons of APP/PS1 mice was improved by β-asarone, meanwhile, β-asarone decreased Aβ deposition and down-regulated Aβ1–42 levels in cortex and hippocampus of APP/PS1 mice brain. Interestingly, the level of RAGE was also significantly down-regulated by β-asarone. Our findings suggest that β-asarone might be effective for the treatment of AD, and the decreasing effects of β-asarone on Aβ might associate with its down-regulation of RAGE. Keywords Alzheimer’s disease β-Asarone Aβ plaques Aβ1-42 Advanced glycation end products