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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...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2017
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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. |
format | Online Article Text |
id | pubmed-5579676 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
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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