Soy Isoflavone Antagonizes the Oxidative Cerebrovascular Injury Induced by β-Amyloid Peptides 1–42 in Rats
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Numerous evidences have shown that the antioxidative properties of soy isoflavone (SIF) have beneficial effects on prophylaxis of neurodegeneration, however, the mechanism is still not fully illustrated. As cerebrovascular dysfunction could initiate a cascade of events leading to pathogenesis of Alzheimer’s disease, we tried to investigate whether SIF could protect the cerebrovascular system due to antagonizing oxidative damage induced by Aβ1–42 in present study. In addition, NF-E2-related factor 2 (Nrf2) signaling pathways in the cerebrovascular tissue of Wistar rats were investigated to identify the potential cerebrovascular protective targets of SIF. Research results showed that SIF reduced the excessive production of nitrotyrosine in cerebrovascular tissue induced by Aβ1–42, and maintained redox homeostasis by increasing the level of GSH and GSH/GSSG. Moreover, SIF could alleviate the down-regulation of Nrf2, γ-glutamylcysteine synthetase, Heme oxygenase-1 expressions in cerebrovascular tissue induced by Aβ1–42 and suppress the increase of Kelch like ECH protein-1 (Keap1). These data suggested that SIF might reduce the cerebrovascular oxidative damage induced by Aβ1–42 through regulating the Nrf2 signaling pathway. The mechanisms of SIF modulating the potential target Nrf2 might be associated with Keap1 expression.
KeywordsSoy isoflavone β-Amyloid peptide 1–42 Cerebrovascular Nrf2 signaling pathway Keap1 Neuroprotection
Transcription factor NF-E2-related factor2
Kelch like ECH protein-1
Reduced glutathione/oxidized glutathione
The authors appreciate the financial support provided by National Natural Science Foundation of China (No. 81172661 and 81302427), the National High Technology Research and Development Program (863 Program) of China (No. 2010AA023003).
Conflict of interest
The authors declare that there are no conflicts of interest.
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