Fumanjian, a Classic Chinese Herbal Formula, Can Ameliorate the Impairment of Spatial Learning and Memory through Apoptotic Signaling Pathway in the Hippocampus of Rats with Aβ1-40-Induced Alzheimer's Disease

被引:7
|
作者
Hu, Hai-yan [1 ,2 ,3 ]
Cui, Zhi-hui [2 ,3 ]
Li, Hui-qin [2 ,3 ]
Wang, Yi-ru [2 ,3 ]
Chen, Xiang [2 ,3 ]
Li, Ji-huang [2 ,3 ]
Xv, Dong-mei [2 ,3 ]
Zheng, Guo-qing [1 ,2 ,3 ]
机构
[1] Wenzhou Med Univ, Clin Med Coll 2, Wenzhou 325027, Peoples R China
[2] Wenzhou Med Univ, Affiliated Hosp 2, Ctr Neurol & Rehabil, Wenzhou 325027, Peoples R China
[3] Wenzhou Med Univ, Yuying Childrens Hosp, Wenzhou 325027, Peoples R China
基金
中国国家自然科学基金;
关键词
AMYLOID BETA-PROTEIN; CELL-DEATH; NEURONS; STRESS;
D O I
10.1155/2014/942917
中图分类号
R [医药、卫生];
学科分类号
10 ;
摘要
Alzheimer's disease (AD) is the most common form of dementia and lacks disease-altering treatments. Fumanjian (FMJ), a famous classic Chinese herbal prescription for dementia, was first recorded in the Complete Works of Jingyue during the Ming Dynasty. This study aimed to investigate whether FMJ could prevent cognitive deficit and take neuroprotective effects in A beta(1-40)-induced rat model through apoptotic signaling pathway. AD model was established by bilateral injection of A beta(1-40) into hippocampus in rat. All rats were tested for their capabilities of spatial navigation and memorization by Morris water maze. Apoptosis was tested using TUNEL staining in hippocampus neuronal cells; RT-PCR tested expression of Bcl-2 and Bax mRNA; western blotting tested protein level of cleaved caspase-3. After 14 days of treatment, FMJ significantly improved the escape latency and enhanced platform-cross number compared with the A beta(1-40)-injected group (P < 0.05 or P < 0.01). FMJ also significantly decreased number of TUNEL-positive neuronal apoptosis and the expressions of Bax and cleaved Caspase-3 and increased the expression of Bcl-2 (P < 0.01) compared with AD model group. In conclusion, FMJ exerts a protective effect against A beta(1-40)-induced learning and memory deficits and neuronal apoptosis, suggesting that FMJ could be used as a potential therapeutic formula for AD.
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收藏
页数:9
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