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

作者：Yang Cong; Li Xiaoguang; Mo Yousheng; Liu Sijun; Zhao Luguang; Ma Xiaohui; Fang Zhigang; Chen Junli; Chen Yunbo; Yu Xuhua; Fang Shuhuan; Zhang Yongbin; Xian Shaoxiang^*; Wang Qi^*

来源：Cellular and Molecular Neurobiology, 2016, 36(1): 121-130.

DOI：10.1007/s10571-015-0226-2

• Alzheimer's disease
• beta-Asarone
• A beta plaques
• A beta 1-42
• Advanced glycation end products

Elevated beta-amyloid (A beta) 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 A beta-induced perturbation in AD, and blockade of RAGE significantly alleviates synaptic injury. Our previous study has suggested that beta-asarone could reduce neuronal apoptosis and improve memory deficits in beta-amyloid precursor protein and presenilin-1 (APP/PS1) double transgenic AD-model mice. In the present study, we evaluated the effects of beta-asarone on amyloidosis in APP/PS1 mice. We found that the survival of neurons of APP/PS1 mice was improved by beta-asarone, meanwhile, beta-asarone decreased A beta deposition and down-regulated A beta 1-42 levels in cortex and hippocampus of APP/PS1 mice brain. Interestingly, the level of RAGE was also significantly down-regulated by beta-asarone. Our findings suggest that beta-asarone might be effective for the treatment of AD, and the decreasing effects of beta-asarone on A beta might associate with its down-regulation of RAGE.

• 单位
  广州中医药大学