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• W2936680690 abstract "Background/Aims . Alzheimer’s disease (AD) is the most common neurodegenerative disease, and all researchers working in this field agree that oxidative stress is intimately associated with Alzheimer disease. In this study, we hypothesized that glutamine (Gln) offers protection against oxidative stress injury in SAMP8 mice as well as the underlying mechanism. Methods . The SAMP8 mice received glutamine intragastrically for 8 consecutive weeks to evaluate the protective effect of glutamine on oxidative stress in AD mice involving Wnt3a/ β -catenin signaling pathway. In addition, rat pheochromocytoma tumor cell line PC12 was pretreated with 32 μ M glutamine for 2 h followed by 24 h incubation with 40 μ M A β 25-35 to obtain in vitro data. Results . In vivo the administration of glutamine was found to ameliorate behavioral deficits and neuron damage, increase superoxide dismutase (SOD) and glutathione peroxidase (GSH-XP) activity, reduce the malondialdehyde (MDA) content, and activate the Wnt3a/ β -catenin signaling pathway in SAMP8 mice. In vitro glutamine treatment decreased the toxicity of A β 25-35 on PC12 cells and prevented apoptosis. Additionally, glutamine treatment increased SOD and GSH-XP activity and decreased MDA content and increased Wnt3a and β -catenin protein levels. Interestingly, the DKK-1 (Wnt3a/ β -catenin pathway inhibitor) decreased the antioxidant capacity of glutamine in A β 25-35-treated PC12 cells. Conclusion . This study suggests that glutamine could protect against oxidative stress-induced injury in AD mice via the Wnt3a/ β -catenin signaling pathway." @default.
• W2936680690 created "2019-04-25" @default.
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• W2936680690 date "2019-04-16" @default.
• W2936680690 modified "2023-10-16" @default.
• W2936680690 title "Glutamine Improves Oxidative Stress through the Wnt3a/<i>β</i>-Catenin Signaling Pathway in Alzheimer’s Disease In Vitro and In Vivo" @default.
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• W2936680690 doi "https://doi.org/10.1155/2019/4690280" @default.
• W2936680690 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6500677" @default.
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