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Hesperidin Protects SH−SY5Y Neuronal Cells against High Glucose−Induced Apoptosis via Regulation of MAPK Signaling

Neurodegenerative diseases are associated with neuronal cell death through apoptosis. Apoptosis is tightly associated with the overproduction of reactive oxygen species (ROS), and high glucose levels contribute to higher oxidative stress in diabetic patients. Hesperidin, a natural active compound, h...

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Autores principales: Lim, Chaemoon, Zhen, Ao Xuan, Ok, Sungwoo, Fernando, Pincha Devage Sameera Madushan, Herath, Herath Mudiyanselage Udari Lakmini, Piao, Mei Jing, Kang, Kyoung Ah, Hyun, Jin Won
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9495902/
https://www.ncbi.nlm.nih.gov/pubmed/36139782
http://dx.doi.org/10.3390/antiox11091707
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author Lim, Chaemoon
Zhen, Ao Xuan
Ok, Sungwoo
Fernando, Pincha Devage Sameera Madushan
Herath, Herath Mudiyanselage Udari Lakmini
Piao, Mei Jing
Kang, Kyoung Ah
Hyun, Jin Won
author_facet Lim, Chaemoon
Zhen, Ao Xuan
Ok, Sungwoo
Fernando, Pincha Devage Sameera Madushan
Herath, Herath Mudiyanselage Udari Lakmini
Piao, Mei Jing
Kang, Kyoung Ah
Hyun, Jin Won
author_sort Lim, Chaemoon
collection PubMed
description Neurodegenerative diseases are associated with neuronal cell death through apoptosis. Apoptosis is tightly associated with the overproduction of reactive oxygen species (ROS), and high glucose levels contribute to higher oxidative stress in diabetic patients. Hesperidin, a natural active compound, has been reported to scavenge free radicals. Only a few studies have explored the protective effects of hesperidin against high glucose−induced apoptosis in SH−SY5Y neuronal cells. Glucose stimulated neuronal cells to generate excessive ROS and caused DNA damage. In addition, glucose triggered endoplasmic reticulum stress and upregulated cytoplasmic as well as mitochondrial calcium levels. Hesperidin inhibited glucose−induced ROS production and mitigated the associated DNA damage and endoplasmic reticulum stress. The downregulation of antiapoptotic protein Bcl−2 following glucose treatment was reversed by a hesperidin treatment. Furthermore, hesperidin repressed the glucose−induced Bcl−2−associated X protein, cleaved caspase−9, and cleaved caspase−3. Hesperidin also suppressed the glucose−induced phosphorylation of extracellular signal−regulated kinase and c−Jun N−terminal kinase. The current results confirmed that hesperidin could protect neuronal cells against glucose−induced ROS. Mechanistically, hesperidin was shown to promote cell viability via attenuation of the mitogen−activated protein kinase signaling pathway.
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spelling pubmed-94959022022-09-23 Hesperidin Protects SH−SY5Y Neuronal Cells against High Glucose−Induced Apoptosis via Regulation of MAPK Signaling Lim, Chaemoon Zhen, Ao Xuan Ok, Sungwoo Fernando, Pincha Devage Sameera Madushan Herath, Herath Mudiyanselage Udari Lakmini Piao, Mei Jing Kang, Kyoung Ah Hyun, Jin Won Antioxidants (Basel) Article Neurodegenerative diseases are associated with neuronal cell death through apoptosis. Apoptosis is tightly associated with the overproduction of reactive oxygen species (ROS), and high glucose levels contribute to higher oxidative stress in diabetic patients. Hesperidin, a natural active compound, has been reported to scavenge free radicals. Only a few studies have explored the protective effects of hesperidin against high glucose−induced apoptosis in SH−SY5Y neuronal cells. Glucose stimulated neuronal cells to generate excessive ROS and caused DNA damage. In addition, glucose triggered endoplasmic reticulum stress and upregulated cytoplasmic as well as mitochondrial calcium levels. Hesperidin inhibited glucose−induced ROS production and mitigated the associated DNA damage and endoplasmic reticulum stress. The downregulation of antiapoptotic protein Bcl−2 following glucose treatment was reversed by a hesperidin treatment. Furthermore, hesperidin repressed the glucose−induced Bcl−2−associated X protein, cleaved caspase−9, and cleaved caspase−3. Hesperidin also suppressed the glucose−induced phosphorylation of extracellular signal−regulated kinase and c−Jun N−terminal kinase. The current results confirmed that hesperidin could protect neuronal cells against glucose−induced ROS. Mechanistically, hesperidin was shown to promote cell viability via attenuation of the mitogen−activated protein kinase signaling pathway. MDPI 2022-08-30 /pmc/articles/PMC9495902/ /pubmed/36139782 http://dx.doi.org/10.3390/antiox11091707 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/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 (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Lim, Chaemoon
Zhen, Ao Xuan
Ok, Sungwoo
Fernando, Pincha Devage Sameera Madushan
Herath, Herath Mudiyanselage Udari Lakmini
Piao, Mei Jing
Kang, Kyoung Ah
Hyun, Jin Won
Hesperidin Protects SH−SY5Y Neuronal Cells against High Glucose−Induced Apoptosis via Regulation of MAPK Signaling
title Hesperidin Protects SH−SY5Y Neuronal Cells against High Glucose−Induced Apoptosis via Regulation of MAPK Signaling
title_full Hesperidin Protects SH−SY5Y Neuronal Cells against High Glucose−Induced Apoptosis via Regulation of MAPK Signaling
title_fullStr Hesperidin Protects SH−SY5Y Neuronal Cells against High Glucose−Induced Apoptosis via Regulation of MAPK Signaling
title_full_unstemmed Hesperidin Protects SH−SY5Y Neuronal Cells against High Glucose−Induced Apoptosis via Regulation of MAPK Signaling
title_short Hesperidin Protects SH−SY5Y Neuronal Cells against High Glucose−Induced Apoptosis via Regulation of MAPK Signaling
title_sort hesperidin protects sh−sy5y neuronal cells against high glucose−induced apoptosis via regulation of mapk signaling
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9495902/
https://www.ncbi.nlm.nih.gov/pubmed/36139782
http://dx.doi.org/10.3390/antiox11091707
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