Genistein inhibits Aβ25–35‐induced SH‐SY5Y cell damage by modulating the expression of apoptosis‐related proteins and Ca2+ influx through ionotropic glutamate receptors

In this study, we investigated the protective effects of genistein against SH‐SY5Y cell damage induced by β‐amyloid 25–35 peptide (Aβ 25–35 ) and the underlying mechanisms. Aβ‐induced neuronal death, apoptosis, glutamate receptor subunit expression, Ca 2+ 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 Aβ 25–35 . In addition, genistein reversed the Aβ 25–35 ‐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. Aβ 25–35 ‐induced changes in Ca 2+ 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 Aβ 25–35 ‐induced damage in SH‐SY5Y cells, possibly by regulating the expression of apoptosis‐related proteins and Ca 2+ influx through ionotropic glutamate receptors.