Soy isoflavone glycitein protects against beta amyloid-induced toxicity and oxidative stress in transgenic Caenorhabditis elegans -: art. no. 54

被引:120
作者
Gutierrez-Zepeda, A
Santell, R
Wu, ZX
Brown, M
Wu, YJ
Khan, I
Link, CD
Zhao, BL
Luo, Y [1 ]
机构
[1] Univ So Mississippi, Dept Biol Sci, Hattiesburg, MS 39406 USA
[2] Alcorn State Univ, Dept Human Sci, Alcorn, MS 39096 USA
[3] Natl Ctr Nat Prod Res, Sch Pharm, Oxford, MS 38655 USA
[4] Univ Colorado, Inst Behav Genet, Boulder, CO 80309 USA
[5] Acad Sinica, Inst Biophys, Ctr Brain & Cognit Sci, Lab Visual Informat Proc, Beijing 100101, Peoples R China
[6] Univ Maryland, Sch Pharm, Dept Pharmaceut Sci, Baltimore, MD 21201 USA
关键词
D O I
10.1186/1471-2202-6-54
中图分类号
Q189 [神经科学];
学科分类号
071006 [神经生物学];
摘要
Background: Epidemiological studies have associated estrogen replacement therapy with a lower risk of developing Alzheimer's disease, but a higher risk of developing breast cancer and certain cardiovascular disorders. The neuroprotective effect of estrogen prompted us to determine potential therapeutic impact of soy-derived estrogenic compounds. Transgenic C. elegans, that express human beta amyloid (A beta), were fed with soy derived isoflavones genistein, daidzein and glycitein ( 100 mu g/ml) and then examined for A beta-induced paralysis and the levels of reactive oxygen species. Results: Among the three compounds tested, only glycitein alleviated A beta expression- induced paralysis in the transgenic C. elegans. This activity of glycitein correlated with a reduced level of hydrogen peroxide in the transgenic C. elegans. In vitro scavenging effects of glycitein on three types of reactive oxygen species confirmed its antioxidant properties. Furthermore, the transgenic C. elegans fed with glycitein exhibited reduced formation of beta amyloid. Conclusion: These findings suggest that a specific soy isoflavone glycitein may suppress A beta toxicity through combined antioxidative activity and inhibition of A beta deposition, thus may have therapeutic potential for prevention of A beta associated neurodegenerative disorders.
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页数:9
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