β-Asarone Mitigates Amyloidosis and Downregulates RAGE in a Transgenic Mouse Model of Alzheimer's Disease.
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.
Institute of Clinical Pharmacology, Guangzhou University of Chinese Medicine, Guangzhou, 510405, China.
Cong
C
Yang
Institute of Clinical Pharmacology, Guangzhou University of Chinese Medicine, Guangzhou, 510405, China.
Xiaoguang
X
Li
Institute of Clinical Pharmacology, Guangzhou University of Chinese Medicine, Guangzhou, 510405, China.
Yousheng
Y
Mo
Institute of Clinical Pharmacology, Guangzhou University of Chinese Medicine, Guangzhou, 510405, China.
Sijun
S
Liu
Institute of Clinical Pharmacology, Guangzhou University of Chinese Medicine, Guangzhou, 510405, China.
Luguang
L
Zhao
Institute of Clinical Pharmacology, Guangzhou University of Chinese Medicine, Guangzhou, 510405, China.
Xiaohui
X
Ma
Institute of Clinical Pharmacology, Guangzhou University of Chinese Medicine, Guangzhou, 510405, China.
Zhigang
Z
Fang
Institute of Clinical Pharmacology, Guangzhou University of Chinese Medicine, Guangzhou, 510405, China.
Junli
J
Chen
Institute of Clinical Pharmacology, Guangzhou University of Chinese Medicine, Guangzhou, 510405, China.
Yunbo
Y
Chen
Institute of Clinical Pharmacology, Guangzhou University of Chinese Medicine, Guangzhou, 510405, China.
Xuhua
X
Yu
Institute of Clinical Pharmacology, Guangzhou University of Chinese Medicine, Guangzhou, 510405, China.
Shuhuan
S
Fang
Laboratory of Experimental Animal, Guangzhou University of Chinese Medicine, Guangzhou, 510405, China.
Yongbin
Y
Zhang
Chinese Internal Medicine, Guangzhou University of Chinese Medicine, Guangzhou, 510405, China. zhongyfy@126.com.
Shaoxiang
S
Xian
Institute of Clinical Pharmacology, Guangzhou University of Chinese Medicine, Guangzhou, 510405, China. wqitcm@qq.com.
Qi
Q
Wang
D000081248:Allylbenzene Derivatives; D000544:Alzheimer Disease / Q000150:complications / Q000188:drug therapy* / Q000473:pathology; D016229:Amyloid beta-Peptides / Q000378:metabolism; D000686:Amyloidosis / Q000150:complications / Q000188:drug therapy* / Q000473:pathology; D000818:Animals; D000840:Anisoles / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D002470:Cell Survival / Q000187:drug effects; D002540:Cerebral Cortex / Q000473:pathology; D004195:Disease Models, Animal; D015536:Down-Regulation / Q000187:drug effects*; D006624:Hippocampus / Q000473:pathology; D008822:Mice, Transgenic; D009474:Neurons / Q000187:drug effects / Q000473:pathology; D058225:Plaque, Amyloid / Q000150:complications / Q000188:drug therapy / Q000473:pathology; D053764:Presenilin-1 / Q000378:metabolism; D000067759:Receptor for Advanced Glycation End Products / Q000378:metabolism*
C000593873:Ager protein, mouse; D000081248:Allylbenzene Derivatives; D016229:Amyloid beta-Peptides; D000840:Anisoles; D053764:Presenilin-1; D000067759:Receptor for Advanced Glycation End Products; C012195:asarone
Advanced glycation end products; Alzheimer’s disease; Aβ plaques; Aβ1-42; β-Asarone