Protective Effects of Fibroblast Growth Factor 21 Against Amyloid-Beta1–42-Induced Toxicity in SH-SY5Y Cells

Protective Effects of Fibroblast Growth Factor 21 Against Amyloid-Beta1–42-Induced Toxicity in... Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by the progressive loss of cholinergic neurons. Amyloid beta is a misfolded protein that represents one of the key pathological hallmarks of AD. Numerous studies have shown that Aβ 1– induces oxidative damage, neuroinflammation, and apoptosis, leading to cognitive decline in AD. Recently, fibroblast growth factor 21 (FGF21) has been suggested to be a potential regulator of oxidative stress in mammalian cells. FGF21 has been shown to improve insulin sensitivity, reduce hyperglycemia, increase adipose tissue glucose uptake and lipolysis, and decrease body fat and weight loss by enhancing energy expenditure. In this study, we investigated the effect of FGF21 Aβ toxicity in SH-SY5Y 1–42 neuroblastoma cells. Our data shows that FGF21 significantly decreased Aβ 42-induced toxic effects and repressed oxidative 1− stress and apoptosis in cells exposed to Aβ peptide. Our investigation also confirmed that FGF21 pretreatment favorably 1–42 affects HSP90/TLR4/NF-κB signaling pathway. Therefore, FGF21 represents a viable therapeutic strategy to abrogate Aβ - 1–42 induced cellular inflammation and apoptotic death in the SH-SY5Y neuroblastoma cells. . . . . . Keywords Alzheimer’sdisease Amyloid beta 42 Neuroblastoma Oxidative stress Neuroinflammation FGF21 Introduction readily form abnormal aggregates with various properties, in- cluding http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Neurotoxicity Research Springer Journals

Protective Effects of Fibroblast Growth Factor 21 Against Amyloid-Beta1–42-Induced Toxicity in SH-SY5Y Cells

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Publisher
Springer Journals
Copyright
Copyright © 2018 by Springer Science+Business Media, LLC, part of Springer Nature
Subject
Biomedicine; Neurosciences; Neurology; Neurochemistry; Pharmacology/Toxicology; Neurobiology; Cell Biology
ISSN
1029-8428
eISSN
1476-3524
D.O.I.
10.1007/s12640-018-9914-2
Publisher site
See Article on Publisher Site

Abstract

Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by the progressive loss of cholinergic neurons. Amyloid beta is a misfolded protein that represents one of the key pathological hallmarks of AD. Numerous studies have shown that Aβ 1– induces oxidative damage, neuroinflammation, and apoptosis, leading to cognitive decline in AD. Recently, fibroblast growth factor 21 (FGF21) has been suggested to be a potential regulator of oxidative stress in mammalian cells. FGF21 has been shown to improve insulin sensitivity, reduce hyperglycemia, increase adipose tissue glucose uptake and lipolysis, and decrease body fat and weight loss by enhancing energy expenditure. In this study, we investigated the effect of FGF21 Aβ toxicity in SH-SY5Y 1–42 neuroblastoma cells. Our data shows that FGF21 significantly decreased Aβ 42-induced toxic effects and repressed oxidative 1− stress and apoptosis in cells exposed to Aβ peptide. Our investigation also confirmed that FGF21 pretreatment favorably 1–42 affects HSP90/TLR4/NF-κB signaling pathway. Therefore, FGF21 represents a viable therapeutic strategy to abrogate Aβ - 1–42 induced cellular inflammation and apoptotic death in the SH-SY5Y neuroblastoma cells. . . . . . Keywords Alzheimer’sdisease Amyloid beta 42 Neuroblastoma Oxidative stress Neuroinflammation FGF21 Introduction readily form abnormal aggregates with various properties, in- cluding

Journal

Neurotoxicity ResearchSpringer Journals

Published: Jun 5, 2018

References

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