Genistein protects against amyloid‐beta‐induced toxicity in SH‐SY5Y cells by regulation of Akt and Tau phosphorylation

• DOI: 10.1002/ptr.6560
• Publication Date: 2019-12-04T00:55:56Z
• Authors: Fernanda dos Sant...; Bárbara Paranhos ...; Mariana Maier Gae...; Fernando Kreutz; Fátima Theresinha...; Christianne Gazza...; Vera Maria Treis ...
• Keywords: Hyperphosphorylation; Tau protein; SH-SY5Y; Amyloid beta

Alzheimer's disease is a neurodegenerative disorder characterized by extracellular deposition of amyloid‐β (Aβ) peptide and hyperphosphorylation Tau protein, which ultimately leads to the formation intracellular neurofibrillary tangles cell death. Increasing evidence indicates that genistein, soy isoflavone, has neuroprotective effects against Aβ‐induced toxicity. However, molecular mechanisms involved in its neuroprotection are not well understood. In this study, we have established neuronal damage model using retinoic‐acid differentiated SH‐SY5Y cells treated with different concentrations Aβ 25–35 investigate effect genistein death possible involvement protein kinase B (PKB, also termed Akt), glycogen synthase 3β (GSK‐3β), as an underlying mechanism neuroprotection. Differentiated were pre‐treated for 24 hr (1 10 nM) exposed (25 μM), found partially inhibited induced death, primarily apoptosis. Furthermore, protective was associated inhibition Akt inactivation hyperphosphorylation. These findings reinforce toxicity provide may involve regulation proteins.