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Flavonoids Protect Cerebrovascular Endothelial Cells through Nrf2 and PI3K from β-Amyloid Peptide-Induced Oxidative Damage

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β-amyloid peptides (Aβ ) induced cerebrovascular dysfunction has been recognized as a vital factor involved in the pathogenesis of neurodegeneration. Genistein, a flavonoid, has antioxidative properties to prevent neurodegeneration induced by β-amyloid peptides. In this study, we were investigating whether genistein could antagonize oxidative damage induced by β-amyloid peptide 25-35 (Aβ25-35) in bEND.3 cells, and also identifying the potential neuroprotective targets of genistein. Vitamin E was used as the positive control. The bEND.3 cells were pre-incubated with/out genistein or vitamin E for 2 h followed by the incubation with 25 μM A 25-35 for another 24 h. The reactive oxygen species (ROS), nitrotyrosine, cell redox state, mRNA or protein expressions of the factors on Nrf2 signaling pathway were measured after Aβ25-35 treatment. The results showed that genistein alleviated the increase of ROS and nitrotyrosine production induced by Aβ25-35, and maintained bEND.3 cell redox state by increasing GSH level and GSH/GSSG. Genistein could reverse the down-regulation of total protein and mRNA expression of NF-E2-related factor 2 (Nrf2), nuclear Nrf2, -&gamma glutamylcysteine synthetase (γ-GCS), phosphatidylinositol 3-kinase (PI3K) induced by Aβ25-35; while PI3K inhibitor LY294002 could attenuate the activation effects of genistein on Nrf2, especially for the promotion of nuclear translocation. These results suggested that genistein could protect cerebrovascular endothelial cells from Aβ25-35-induced oxidative damage. The potential mechanisms might be associated with the activation of Nrf2 signaling pathway by modulating PI3K activity.

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Keywords: Alzheimer's disease; Genistein; Nrf2 signaling pathway; PI3K; SIF; antiinflammatory; bEND.3; cerebrovascular; cerebrovascular endothelial cells; flavonoids; glial cells; neuropathological; neuroprotection; oxidative damage; redox; β-amyloid peptide 25-35

Document Type: Research Article

Publication date: February 1, 2012

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  • Current Neurovascular Research (CNR) provides a cross platform for the publication of scientifically rigorous research that addresses disease mechanisms of both neuronal and vascular origins in neuroscience. The journal serves as an international forum for the publication of novel and pioneering original work as well as timely neuroscience research reviews in the disciplines of cell developmental disorders, plasticity, and degeneration that bridge the gap between basic science research and clinical discovery. CNR emphasizes the elucidation of disease mechanisms, both cellular and molecular, which can impact the development of unique therapeutic strategies for neuronal and vascular disorders.
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