期刊
JOURNAL OF NEUROSCIENCE RESEARCH
卷 97, 期 4, 页码 492-505出版社
WILEY
DOI: 10.1002/jnr.24357
关键词
Alzheimer's disease; antioxidative stress; ARE; Nrf2; oxidative stress; RRID: AB_944418; RRID: AB_1603750; RRID: AB_2118663; RRID: AB_2222860; RRID: SCR_002798; RRID: SCR_002865; RRID: MGI:5656552; RRID: AB_11128526; RRID: AB_955447
资金
- Key Project of the National Natural Science Foundation of China [81530036]
- National Key Scientific Instrument and Equipment Development Project [31627803]
- Mission Program of Beijing Municipal Administration of Hospitals [SML20150801]
- Beijing Brain Initiative from Beijing Municipal Science & Technology Commission [Z161100000216137]
- CHINA-CANADA Joint Initiative on Alzheimer's Disease and Related Disorders [81261120571]
- Beijing Municipal Commission of Health and Family Planning [PXM2017_026283_000002]
Oxidative stress refers to an imbalance between oxidative and antioxidative systems due to environmental factors. Although oxidative stress is implicated in the pathogenesis of Alzheimer's disease (AD), its precise role is not yet understood. We aimed to investigate the pathogenic mechanisms of the oxidative stress by using in vitro cultured neurons and in vivo AD models of PS1V97L-transgenic (Tg) mice. Our results showed that when oxidative stress became increasingly evident, the endogenous protective pathway of nuclear factor E2-related factor 2 (Nrf2)/antioxidant response element (ARE) decreased in 10-month-old PS1V97L-Tg mice. Activating the Nrf2/ARE pathway suppressed oxidative stress, decreased amyloid-beta (A beta), and improved the cognitive function of the PS1V97L-Tg mice. In contrast, blocking the Nrf2/ARE pathway augmented oxidative injury and decreased the cell viability of PS1V97L-Tg neurons. Our results highlight the role of the Nrf2/ARE pathway in regulating oxidative stress of the PS1V97L-Tg mice and may indicate a potential therapeutic avenue for AD treatment.
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