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Inhibitory Effect of Lycopene on Amyloid-β-Induced Apoptosis in Neuronal Cells

Alzheimer′s disease (AD) is a fatal neurodegenerative disease. Brain amyloid-β deposition is a crucial feature of AD, causing neuronal cell death by inducing oxidative damage. Reactive oxygen species (ROS) activate NF-κB, which induces expression of Nucling. Nucling is a pro-apoptotic factor recruit...

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Autores principales: Hwang, Sinwoo, Lim, Joo Weon, Kim, Hyeyoung
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5579676/
https://www.ncbi.nlm.nih.gov/pubmed/28813012
http://dx.doi.org/10.3390/nu9080883
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author Hwang, Sinwoo
Lim, Joo Weon
Kim, Hyeyoung
author_facet Hwang, Sinwoo
Lim, Joo Weon
Kim, Hyeyoung
author_sort Hwang, Sinwoo
collection PubMed
description Alzheimer′s disease (AD) is a fatal neurodegenerative disease. Brain amyloid-β deposition is a crucial feature of AD, causing neuronal cell death by inducing oxidative damage. Reactive oxygen species (ROS) activate NF-κB, which induces expression of Nucling. Nucling is a pro-apoptotic factor recruiting the apoptosome complex. Lycopene is an antioxidant protecting from oxidative stress-induced cell damage. We investigated whether lycopene inhibits amyloid-β-stimulated apoptosis through reducing ROS and inhibiting mitochondrial dysfunction and NF-κB-mediated Nucling expression in neuronal SH-SY5Y cells. We prepared cells transfected with siRNA for Nucling or nontargeting control siRNA to determine the role of Nucling in amyloid-β-induced apoptosis. The amyloid-β increased intracellular and mitochondrial ROS levels, apoptotic indices (p53, Bax/Bcl-2 ratio, caspase-3 cleavage), NF-kB activation and Nucling expression, while cell viability, mitochondrial membrane potential, and oxygen consumption rate decreased in SH-SY5Y cells. Lycopene inhibited these amyloid-β-induced alterations. However, amyloid-β did not induce apoptosis, determined by cell viability and apoptotic indices (p53, Bax/Bcl-2 ratio, caspase-3 cleavage), in the cells transfected with siRNA for Nucling. Lycopene inhibited apoptosis by reducing ROS, and by inhibiting mitochondrial dysfunction and NF-κB-target gene Nucling expression in neuronal cells. Lycopene may be beneficial for preventing oxidative stress-mediated neuronal death in patients with neurodegeneration.
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spelling pubmed-55796762017-09-06 Inhibitory Effect of Lycopene on Amyloid-β-Induced Apoptosis in Neuronal Cells Hwang, Sinwoo Lim, Joo Weon Kim, Hyeyoung Nutrients Article Alzheimer′s disease (AD) is a fatal neurodegenerative disease. Brain amyloid-β deposition is a crucial feature of AD, causing neuronal cell death by inducing oxidative damage. Reactive oxygen species (ROS) activate NF-κB, which induces expression of Nucling. Nucling is a pro-apoptotic factor recruiting the apoptosome complex. Lycopene is an antioxidant protecting from oxidative stress-induced cell damage. We investigated whether lycopene inhibits amyloid-β-stimulated apoptosis through reducing ROS and inhibiting mitochondrial dysfunction and NF-κB-mediated Nucling expression in neuronal SH-SY5Y cells. We prepared cells transfected with siRNA for Nucling or nontargeting control siRNA to determine the role of Nucling in amyloid-β-induced apoptosis. The amyloid-β increased intracellular and mitochondrial ROS levels, apoptotic indices (p53, Bax/Bcl-2 ratio, caspase-3 cleavage), NF-kB activation and Nucling expression, while cell viability, mitochondrial membrane potential, and oxygen consumption rate decreased in SH-SY5Y cells. Lycopene inhibited these amyloid-β-induced alterations. However, amyloid-β did not induce apoptosis, determined by cell viability and apoptotic indices (p53, Bax/Bcl-2 ratio, caspase-3 cleavage), in the cells transfected with siRNA for Nucling. Lycopene inhibited apoptosis by reducing ROS, and by inhibiting mitochondrial dysfunction and NF-κB-target gene Nucling expression in neuronal cells. Lycopene may be beneficial for preventing oxidative stress-mediated neuronal death in patients with neurodegeneration. MDPI 2017-08-16 /pmc/articles/PMC5579676/ /pubmed/28813012 http://dx.doi.org/10.3390/nu9080883 Text en © 2017 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Hwang, Sinwoo
Lim, Joo Weon
Kim, Hyeyoung
Inhibitory Effect of Lycopene on Amyloid-β-Induced Apoptosis in Neuronal Cells
title Inhibitory Effect of Lycopene on Amyloid-β-Induced Apoptosis in Neuronal Cells
title_full Inhibitory Effect of Lycopene on Amyloid-β-Induced Apoptosis in Neuronal Cells
title_fullStr Inhibitory Effect of Lycopene on Amyloid-β-Induced Apoptosis in Neuronal Cells
title_full_unstemmed Inhibitory Effect of Lycopene on Amyloid-β-Induced Apoptosis in Neuronal Cells
title_short Inhibitory Effect of Lycopene on Amyloid-β-Induced Apoptosis in Neuronal Cells
title_sort inhibitory effect of lycopene on amyloid-β-induced apoptosis in neuronal cells
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5579676/
https://www.ncbi.nlm.nih.gov/pubmed/28813012
http://dx.doi.org/10.3390/nu9080883
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