Neuroprotective effect of sinapic acid in a mouse model of amyloid β1-42 protein-induced Alzheimer's disease

被引:86
作者
Lee, Hyung Eun [1 ,2 ]
Kim, Dong Hyun [1 ,2 ]
Park, Se Jin [1 ,2 ]
Kim, Jong Min [1 ,2 ]
Lee, Young Woo [1 ,2 ]
Jung, Jun Man [1 ,2 ]
Lee, Chang Hwan [1 ,2 ]
Hong, Jin Gyu [1 ,2 ]
Liu, Xiaotong [1 ,2 ]
Cai, Mudan [1 ,2 ]
Park, Keon Ju [1 ]
Jang, Dae Sik [1 ,2 ]
Ryu, Jong Hoon [1 ,2 ]
机构
[1] Kyung Hee Univ, Kyung Hee EW Pharmaceut Res Inst, Coll Pharm, Seoul 130701, South Korea
[2] Kyung Hee Univ, Dept Life & Nanopharmaceut Sci, Seoul 130701, South Korea
关键词
Sinapic acid; Amyloid beta protein; Memory; Alzheimer's disease; Neuroinflammation; NITRIC-OXIDE SYNTHASE; PRECURSOR PROTEIN; PHENOLIC-ACIDS; CELL-DEATH; INCREASES; ACTIVATION; APOPTOSIS; CASPASE-3; COGNITION; DEMENTIA;
D O I
10.1016/j.pbb.2012.08.015
中图分类号
B84 [心理学]; C [社会科学总论]; Q98 [人类学];
学科分类号
03 ; 0303 ; 030303 ; 04 ; 0402 ;
摘要
Sinapic acid (SA) is a phenylpropanoid compound with anti-inflammatory and neuroprotective activities. The neuroprotective effects of SA in a mouse model of amyloid beta (A beta)(1-42) protein-induced Alzheimer's disease (AD) were investigated. Mice received a bilateral injection of A beta(1-42) protein into the hippocampus to verify the efficacy of SA. Mice were treated with SA (10 mg/kg/day, p.o.) for 7 days beginning immediately after A beta(1-42) protein injection, and an acquisition trial of the passive avoidance task was conducted 1 h after the last administration of SA. Retention trial was conducted 24 h after the acquisition trial, and mice were sacrificed for immunohistochemistry immediately after the retention trial. SA rescued neuronal cell death in the hippocampal CA1 region and also attenuated the increase of iNOS expression, glial cell activations and nitrotyrosine expressions induced by A beta(1-42) protein. SA significantly attenuated memory impairment in the passive avoidance task. These results suggest that SA ameliorated A beta(1-42) protein-related pathology including neuronal cell death and cognitive dysfunction via its anti-oxidative and anti-inflammatory activities, and may be an efficacious treatment for AD. (C) 2012 Elsevier Inc. All rights reserved.
引用
收藏
页码:260 / 266
页数:7
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