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Alzheimer's disease (AD), a very common neurodegenerative disorder, is mainly characterized by the deposition of β-amyloid protein (Aβ) and extensive neuronal cell death. Currently, there are no satisfactory therapeutic approaches for AD. Although neuroprotective effects of genistein against Aβ-induced toxicity have been reported, the underlying molecular mechanisms remain unclear. Furthermore, the PI3K/Akt/Nrf2 signaling pathway is associated with AD. The aim of the study was to investigate whether genistein can modulate Nrf2/HO-1/PI3K signaling to treat AD.MATERIALS AND METHODSCell viability assay, the measurement of heme oxygenase-1 (HO-1) expression by reverse transcription-polymerase chain reaction (RT-qPCR), and western blot were performed on the SH-SY5Y cells induced by Aβ25-35 in response to the treatment of genistein. Moreover, PI3K p85 phosphorylation was measured.RESULTSGenistein enhanced the HO-1expression at both the mRNA and protein levels, as well as the PI3K p85 phosphorylation level. In addition, genistein increased the survival of SH-SY5Y cells treated with Aβ25-35via HO-1 signaling. However, following transfection with Nrf2 small interfering RNA (siRNA) and treatment with LY294002, an inhibitor of PI3K p85, genistein could not upregulate HO-1 to exert neuroprotective effects on SH-SY5Y cells treated with Aβ25-35.CONCLUSIONSThese results suggest that genistein exerts a neuroprotective effect on SH-SY5Y cells in vitro via Nrf2/HO-1/PI3K signaling, providing a foundation for the application of genistein in the treatment of neurodegenerative diseases related to Nrf2/HO-1/PI3K signaling.

Genistein exerts a cell-protective effect via Nrf2/HO-1/ /PI3K signaling in Ab25-35-induced Alzheimer’s disease models in vitro