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Nrf2 Ablation Promotes Alzheimer’s Disease-Like Pathology in APPPS1 Transgenic Mice: The Role of Neuroinflammation and Oxidative Stress
المؤلفون المشاركون
Yang, Bei
Zhang, Guohua
Zhao, Rui
Ren, Peng
Chen, Jingwei
Li, Bingxuan
Zhang, Mengzhou
Guo, Xiangshen
Chen, Ziyuan
Cheng, Hao
Wang, Pengfei
Wang, Shuaibo
Wang, Ning
Wu, Xu
Ma, Dan
Guan, Dawei
المصدر
Oxidative Medicine and Cellular Longevity
العدد
المجلد 2020، العدد 2020 (31 ديسمبر/كانون الأول 2020)، ص ص. 1-13، 13ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2020-05-11
دولة النشر
مصر
عدد الصفحات
13
التخصصات الرئيسية
الملخص EN
Introduction.
Alzheimer’s disease (AD), the most common neurodegenerative disorder, is characterized by the accumulation of amyloid-β (Aβ) peptide and hyperphosphorylated tau protein.
Accumulating evidence has revealed that the slow progressive deterioration of AD is associated with oxidative stress and chronic inflammation in the brain.
Nuclear factor erythroid 2- (NF-E2-) related factor 2 (Nrf2), which acts through the Nrf2/ARE pathway, is a key regulator of the antioxidant and anti-inflammatory response.
Although recent data show a link between Nrf2 and AD-related cognitive decline, the mechanism is still unknown.
Thus, we explored how Nrf2 protects brain cells against the oxidative stress and inflammation of AD in a mouse model of AD (APP/PS1 transgenic (AT) mice) with genetic removal of Nrf2.
Methods.
The spatial learning and memory abilities of 12-month-old transgenic mice were evaluated using a Morris water maze test.
Hippocampal levels of Nrf2, Aβ, and p-tauS404 and of astrocytes and microglia were determined by immunostaining.
Inflammatory cytokines were determined by ELISA and quantitative real-time polymerase chain reaction (qRT-PCR).
Oxidative stress was measured by 8-hydroxydeoxyguanosine immunohistochemistry, and the antioxidant response was determined by qRT-PCR.
Results.
The spatial learning and memory abilities of AT mice were impaired after Nrf2 deletion.
Aβ and p-tauS404 accumulation was increased in the hippocampus of AT/Nrf2-KO mice.
Astroglial and microglial activation was exacerbated, followed by upregulation of the proinflammatory cytokines IL-1β, IL-6, and TNF-α.
Conclusion.
Our present results show that Nrf2 deficiency aggravates AD-like pathology in AT mice.
This phenotype was associated with increased levels of oxidative and proinflammatory markers, which suggests that the Nrf2 pathway may be a promising therapeutic target for AD.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Ren, Peng& Chen, Jingwei& Li, Bingxuan& Zhang, Mengzhou& Yang, Bei& Guo, Xiangshen…[et al.]. 2020. Nrf2 Ablation Promotes Alzheimer’s Disease-Like Pathology in APPPS1 Transgenic Mice: The Role of Neuroinflammation and Oxidative Stress. Oxidative Medicine and Cellular Longevity،Vol. 2020, no. 2020, pp.1-13.
https://search.emarefa.net/detail/BIM-1204128
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Ren, Peng…[et al.]. Nrf2 Ablation Promotes Alzheimer’s Disease-Like Pathology in APPPS1 Transgenic Mice: The Role of Neuroinflammation and Oxidative Stress. Oxidative Medicine and Cellular Longevity No. 2020 (2020), pp.1-13.
https://search.emarefa.net/detail/BIM-1204128
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Ren, Peng& Chen, Jingwei& Li, Bingxuan& Zhang, Mengzhou& Yang, Bei& Guo, Xiangshen…[et al.]. Nrf2 Ablation Promotes Alzheimer’s Disease-Like Pathology in APPPS1 Transgenic Mice: The Role of Neuroinflammation and Oxidative Stress. Oxidative Medicine and Cellular Longevity. 2020. Vol. 2020, no. 2020, pp.1-13.
https://search.emarefa.net/detail/BIM-1204128
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1204128
قاعدة معامل التأثير والاستشهادات المرجعية العربي "ارسيف Arcif"
أضخم قاعدة بيانات عربية للاستشهادات المرجعية للمجلات العلمية المحكمة الصادرة في العالم العربي
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