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Neurochemical Research

, Volume 39, Issue 7, pp 1374–1381 | Cite as

Soy Isoflavone Antagonizes the Oxidative Cerebrovascular Injury Induced by β-Amyloid Peptides 1–42 in Rats

  • Yuan-Di Xi
  • Xiao-Ying Li
  • Huan-Ling Yu
  • Han Jing
  • Wei-Wei Ma
  • Lin-Hong Yuan
  • Dan-Di Zhang
  • Jian Wu
  • Rong Xiao
Original Paper

Abstract

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.

Keywords

Soy isoflavone β-Amyloid peptide 1–42 Cerebrovascular Nrf2 signaling pathway Keap1 Neuroprotection 

Abbreviations

β-Amyloid peptides

AD

Alzheimer’s disease

Nrf2

Transcription factor NF-E2-related factor2

Keap1

Kelch like ECH protein-1

γ-GCS

γ-Glutamylcysteine synthetase

HO-1

Heme oxygenase-1

GSH/GSSG

Reduced glutathione/oxidized glutathione

Notes

Acknowledgments

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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Copyright information

© Springer Science+Business Media New York 2014

Authors and Affiliations

  • Yuan-Di Xi
    • 1
    • 3
  • Xiao-Ying Li
    • 2
  • Huan-Ling Yu
    • 1
    • 3
  • Han Jing
    • 1
    • 3
  • Wei-Wei Ma
    • 1
    • 3
  • Lin-Hong Yuan
    • 1
    • 3
  • Dan-Di Zhang
    • 1
    • 3
  • Jian Wu
    • 2
  • Rong Xiao
    • 1
    • 3
  1. 1.School of Public HealthCapital Medical UniversityBeijingPeople’s Republic of China
  2. 2.Xuanwu HospitalCapital Medical UniversityBeijingPeople’s Republic of China
  3. 3.Beijing Key Laboratory of Environmental ToxicologyCapital Medical UniversityBeijingPeople’s Republic of China

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