Neuroprotective effects of Triticum aestivum L. against β-Amyloid-induced cell death and memory impairments
β-Amyloid (Aβ) is a key component of senile plaques, neuropathological hallmarks of Alzheimer's disease (AD) and has been reported to induce cell death via oxidative stress. This study investigated the protective effects of Triticum aestivum L. (TAL) on Aβ-induced apoptosis in SH-SY5Y cells and...
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Published in | Phytotherapy research Vol. 24; no. 1; pp. 76 - 84 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Chichester, UK
John Wiley & Sons, Ltd
2010
Wiley |
Subjects | |
Online Access | Get full text |
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Summary: | β-Amyloid (Aβ) is a key component of senile plaques, neuropathological hallmarks of Alzheimer's disease (AD) and has been reported to induce cell death via oxidative stress. This study investigated the protective effects of Triticum aestivum L. (TAL) on Aβ-induced apoptosis in SH-SY5Y cells and cognitive dysfunctions in Sprague-Dawley (SD) rats. Cells treated with Aβ exhibited decreased viability and apoptotic features, such as DNA fragmentation, alterations in mitochondria and an increased Bax/Bcl-2 ratio, which were attenuated by TAL extract (TALE) pretreatment. To elucidate the neuroprotective mechanisms of TALE, the study examined Aβ-induced oxidative stress and cellular defense. TALE pretreatment suppressed Aβ-increased intracellular accumulation of reactive oxygen species (ROS) via up-regulation of glutathione, an essential endogenous antioxidant. To further verify the effect of TALE on memory impairments, Aβ or scopolamine was injected in SD rats and a water maze task conducted as a spatial memory test. Aβ or scopolamine treatment increased the time taken to find the platform during training trials, which was decreased by TALE pretreatment. Furthermore, one of the active components of TALE, total dietary fiber also effectively inhibited Aβ-induced cytotoxicity and scopolamine-caused memory deficits. These results suggest that TALE may have preventive and/or therapeutic potential in the management of AD. Copyright © 2009 John Wiley & Sons, Ltd. |
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Bibliography: | http://dx.doi.org/10.1002/ptr.2871 istex:7636471C031BD7780C7C486ADE60A00733B49085 ArticleID:PTR2871 ark:/67375/WNG-1FDVZ2M1-H ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0951-418X 1099-1573 |
DOI: | 10.1002/ptr.2871 |