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Phytoestrogen kaempferol (3,4′,5,7‐tetrahydroxyflavone) protects PC12 and T47D cells from β‐amyloid–induced toxicity
Author(s) -
Roth Adrian,
Schaffner Willy,
Hertel Cornelia
Publication year - 1999
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/(sici)1097-4547(19990801)57:3<399::aid-jnr12>3.0.co;2-w
Subject(s) - phytoestrogens , estrogen receptor , estrogen , agonist , kaempferol , neurodegeneration , fulvestrant , receptor , toxicity , pharmacology , medicine , endocrinology , chemistry , biology , breast cancer , biochemistry , cancer , disease , quercetin , antioxidant
In clinical studies, it has been shown that estrogen replacement therapy in menopause is strongly correlated with a reduced risk of the development of Alzheimer's disease (AD). In in vitro experiments, it was demonstrated that estradiol protects cells against the toxic effects of β‐amyloid, the major component of plaques in brains of AD patients. Therefore, estrogens have become interesting candidates for a possible treatment of neurodegeneration. In plants, a class of compounds has been identified that bind to human estrogen receptor, so‐called phytoestrogens, which are part of our daily diet. Here, we compared the effects of α‐ and β‐estradiol with plant‐derived kaempferol on β‐amyloid peptide–induced toxicity in PC12 neuroblastoma and T47D human breast cancer cells. The present results demonstrate a protective effect of kaempferol comparable to that observed with estradiol. The effects of the weak estrogen receptor agonists α‐estradiol and kaempferol were found to be similar to the effects of the strong estrogen receptor agonist β‐estradiol, suggesting a mode of action independent from the nuclear estrogen receptor. J. Neurosci. Res. 57:399–404, 1999. © 1999 Wiley‐Liss, Inc.