Genistein inhibits Aβ25-35-induced SH-SY5Y cell damage by modulating the expression of apoptosis-related proteins and Ca2+influx through ionotropic glutamate receptors
| Autor: | Li-Xia Li, Bin Heng, Yu-xiang Wang, Di An, Hong-gang Wang, Yan-Qiang Liu, Hui-nan Xu |
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| Rok vydání: | 2018 |
| Předmět: |
Pharmacology
0303 health sciences 030302 biochemistry & molecular biology Glutamate receptor Genistein AMPA receptor medicine.disease Cell biology 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine chemistry 030220 oncology & carcinogenesis medicine Ionotropic glutamate receptor NMDA receptor Receptor Cell damage Ionotropic effect |
| Zdroj: | Phytotherapy Research. 33:431-441 |
| ISSN: | 0951-418X |
| DOI: | 10.1002/ptr.6239 |
| Popis: | In this study, we investigated the protective effects of genistein against SH-SY5Y cell damage induced by β-amyloid 25-35 peptide (Aβ25-35 ) and the underlying mechanisms. Aβ-induced neuronal death, apoptosis, glutamate receptor subunit expression, Ca2+ ion concentration, amino acid transmitter concentration, and apoptosis-related factor expression were evaluated to determine the effects of genistein on Aβ-induced neuronal death and apoptosis. The results showed that genistein increased the survival of SH-SY5Y cells and decreased the level of apoptosis induced by Aβ25-35 . In addition, genistein reversed the Aβ25-35 -induced changes in amino acid transmitters, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptors, and N-methyl-d-aspartate (NMDA) receptor subunits in SH-SY5Y cells. Aβ25-35 -induced changes in Ca2+ and B-cell lymphoma-2 (Bcl-2) and Bcl-2-associated X (Bax) protein and gene levels in cells were also reversed by genistein. Our data suggest that genistein protects against Aβ25-35 -induced damage in SH-SY5Y cells, possibly by regulating the expression of apoptosis-related proteins and Ca2+ influx through ionotropic glutamate receptors. |
| Databáze: | OpenAIRE |
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