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Neuroprotective effect of isoflavones against homocysteine‐mediated neuronal degeneration in SH‐SY5Y cells
Author(s) -
Kwon Young Hye,
Park YounJin,
Jang Yumi
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.924.7
Subject(s) - genistein , isoflavones , neuroprotection , neurotoxicity , neurodegeneration , sh sy5y , unfolded protein response , medicine , oxidative stress , daidzein , endocrinology , chemistry , apoptosis , pharmacology , biology , biochemistry , neuroblastoma , toxicity , cell culture , disease , genetics
Several studies reported that ER stress‐induced homocysteine (Hcy) toxicity may play an important role in the pathogenesis of neurodegeneration. Estrogen as well as isoflavones has been suggested to have the protective effect against the risk of developing neurodegenerative diseases. Therefore, in the present study, we investigated effects of isoflavones (genistein and daidzein) on Hcy‐mediated neurotoxicity in SH‐SY5Y human neuroblastoma cells. Treatment of cells with isoflavones significantly protected cells against Hcy‐mediated apoptosis. We observed significant increase in DNA damage by Hcy, which was alleviated by isoflavones. Isoflavones suppressed Hcy‐mediated ER stress as determined by decreased expressions of the binding protein (BiP) mRNA, spliced X‐box‐protein (Xbp)‐1 mRNAs and C/EBP homologous transcription factor (CHOP) protein. Treatment of cells with isoflavones also significantly inactivated GSK3β and decreased tau hyperphosphorylation. In conclusion, our results demonstrate that isoflavones may alleviate ER stress‐mediated neurodegeneration. This study was supported by a grant from Korea Research Foundation.