机构：[1]School of Public Health, Capital Medical University, No. 10 Xitoutiao, You An Men, Beijing, People’s Republic of China[2]Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing, People’s Republic of China[3]Xuanwu Hospital, Capital Medical University, No. 45 Changchun Street, Beijing, People’s Republic of China首都医科大学宣武医院
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 A beta 1-42 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 A beta 1-42, and maintained redox homeostasis by increasing the level of GSH and GSH/GSSG. Moreover, SIF could alleviate the down-regulation of Nrf2, gamma-glutamylcysteine synthetase, Heme oxygenase-1 expressions in cerebrovascular tissue induced by A beta 1-42 and suppress the increase of Kelch like ECH protein-1 (Keap1). These data suggested that SIF might reduce the cerebrovascular oxidative damage induced by A beta 1-42 through regulating the Nrf2 signaling pathway. The mechanisms of SIF modulating the potential target Nrf2 might be associated with Keap1 expression.
基金：
National Natural Science Foundation of China (No.81172661 and 81302427),
the National High Technology Research and Development Program (863 Program) of China (No.2010AA023003).
第一作者机构：[1]School of Public Health, Capital Medical University, No. 10 Xitoutiao, You An Men, Beijing, People’s Republic of China[2]Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing, People’s Republic of China
共同第一作者：
通讯作者：
通讯机构：[1]School of Public Health, Capital Medical University, No. 10 Xitoutiao, You An Men, Beijing, People’s Republic of China[2]Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing, People’s Republic of China
推荐引用方式(GB/T 7714)：
Yuan-Di Xi,Xiao-Ying Li,Huan-Ling Yu,et al.Soy Isoflavone Antagonizes the Oxidative Cerebrovascular Injury Induced by beta-Amyloid Peptides 1-42 in Rats[J].NEUROCHEMICAL RESEARCH.2014,39(7):1374-1381.doi:10.1007/s11064-014-1319-x.
APA：
Yuan-Di Xi,Xiao-Ying Li,Huan-Ling Yu,Han Jing,Wei-Wei Ma...&Rong Xiao.(2014).Soy Isoflavone Antagonizes the Oxidative Cerebrovascular Injury Induced by beta-Amyloid Peptides 1-42 in Rats.NEUROCHEMICAL RESEARCH,39,(7)
MLA：
Yuan-Di Xi,et al."Soy Isoflavone Antagonizes the Oxidative Cerebrovascular Injury Induced by beta-Amyloid Peptides 1-42 in Rats".NEUROCHEMICAL RESEARCH 39..7(2014):1374-1381
