Amelioration of Alzheimer's disease by neuroprotective effect of sulforaphane in animal model

被引：124

作者：

Kim, Hyunjin Vincent ^{[1
]}

Kim, Hye Yun ^{[1
]}

Ehrlich, Hanna Y. ^{[1
,2
]}

Choi, Seon Young ^{[1
]}

Kim, Dong Jin ^{[1
]}

Kim, YoungSoo ^{[1
]}

机构：

[1] Korea Inst Sci & Technol, Brain Sci Inst, Ctr Neuromed, Seoul, South Korea

[2] Tufts Univ, Dept Biol, Medford, MA USA

来源：

AMYLOID-JOURNAL OF PROTEIN FOLDING DISORDERS | 2013年 / 20卷 / 01期

关键词：

Acute AD animal model; Alzheimer's disease; amyloid-beta; cell viability assay; passive avoidance test; reactive oxygen species; sulforaphane; Y-maze test; BETA-AMYLOID PEPTIDES; SOLID-PHASE SYNTHESIS; OXIDATIVE STRESS; NEUROTOXICITY; PROTEASOME; PROTECTION; AGGREGATION; ACTIVATION; MECHANISMS; OLIGOMERS;

D O I：

10.3109/13506129.2012.751367

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Pathophysiological evidences of AD have indicated that aggregation of A beta is one of the principal causes of neuronal dysfunction, largely by way of inducing oxidative stresses such as free radical formation. We hypothesized that the known antioxidative attribute of SFN could be harnessed in Alzheimer's treatment. SFN is an indirect, potent antioxidant derived from broccoli that has previously been found to stimulate the Nrf2-ARE pathway and facilitate several other cytoprotective mechanisms. In this study, administration of SFN ameliorated cognitive function of A beta-induced AD acute mouse models in Y-maze and passive avoidance behavior tests. Interestingly, we found that the therapeutic effect of SFN did not involve inhibition of A beta aggregation. While the exact mechanism of interaction of SFN in AD has not yet been ascertained, our results suggest that SFN can aid in cognitive impairment and may protect the brain from amyloidogenic damages.

引用

页码：7 / 12

页数：6

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