Danggui-Shaoyao-San and its active fraction JD-30 improve Aβ-induced spatial recognition deficits in mice

被引:60
作者
Hu, Zeng-Yao [1 ]
Liu, Gang [1 ]
Yuan, Hui [1 ]
Yang, Sheng [1 ]
Zhou, Wen-Xia [1 ]
Zhang, Yong-Xiang [1 ]
Qiao, Shan-Yi [1 ]
机构
[1] Beijing Inst Pharmacol & Toxicol, Beijing 100850, Peoples R China
基金
中国国家自然科学基金;
关键词
Danggui-Shaoyao-San; JD-30; beta-Amyloid; Spatial learning and memory; Long-term potentiation; Fibril formation; TOKI-SHAKUYAKU-SAN; LONG-TERM POTENTIATION; RAT HIPPOCAMPAL SLICES; HERBAL MEDICINE; ALZHEIMERS-DISEASE; IMPAIRMENT; MEMORY; THERAPY; MAZE; AREA;
D O I
10.1016/j.jep.2010.01.046
中图分类号
Q94 [植物学];
学科分类号
071001 [植物学];
摘要
Aims of the study: Previous studies showed that Danggui-Shaoyao-San (DSS), a traditional Chinese medicinal prescription, could alleviate cognitive dysfunction of Alzheimer's disease (AD) patients However, the mechanism and substance basis remain unknown JD-30 is a fraction extracted from DSS, whose activity we previously was evaluated beta-Amyloid (A beta) is believed to be a critical etiological factor of AD. We have now examined the effect of DSS and JD-30 on AD model mice induced by A beta, and elucidated the possible mechanism. Materials and methods. Mice were intracerebroventricular injected with the aggregated A beta(25-35) to mimic AD Groups of mice were treated with DSS or JD-30 by intragastric infusion over 2 weeks, and their spatial learning and memory capacities were measured by the Morris water maze procedure The mechanisms were investigated by extracellular microelectrode recordings, and also electron microscopy Results. Our results show that A beta(25-35) induced impairment of spatial learning and memory in mice, as well as inhibition of long-term potentiation (LIP) in the hippocampus The impairments were ameliorated by DSS or JD-30 administration Additionally, JD-30 not only prevented the aggregation of A beta(25-35), but disrupted aggregated A beta(25-35) fibrils Conclusion These results suggest that JD-30 is one of the chief active fractions extracted from DSS by its ability to ameliorate deterioration of cognition, and by blocking and disrupting the aggregation of A beta so that synaptic plasticity was improved, which may be one of the mechanisms involved. (C) 2010 Elsevier Ireland Ltd All rights reserved
引用
收藏
页码:365 / 372
页数:8
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