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Cyanidin Attenuates Methylglyoxal-Induced Oxidative Stress and Apoptosis in INS-1 Pancreatic β-Cells by Increasing Glyoxalase-1 Activity

Recently, the mechanisms responsible for anti-glycation activity of cyanidin and its derivatives on the inhibition of methylglyoxal (MG)-induced protein glycation and advanced glycation-end products (AGEs) as well as oxidative DNA damage were reported. In this study, we investigated the protective e...

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Autores principales: Suantawee, Tanyawan, Thilavech, Thavaree, Cheng, Henrique, Adisakwattana, Sirichai
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7284759/
https://www.ncbi.nlm.nih.gov/pubmed/32384625
http://dx.doi.org/10.3390/nu12051319
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author Suantawee, Tanyawan
Thilavech, Thavaree
Cheng, Henrique
Adisakwattana, Sirichai
author_facet Suantawee, Tanyawan
Thilavech, Thavaree
Cheng, Henrique
Adisakwattana, Sirichai
author_sort Suantawee, Tanyawan
collection PubMed
description Recently, the mechanisms responsible for anti-glycation activity of cyanidin and its derivatives on the inhibition of methylglyoxal (MG)-induced protein glycation and advanced glycation-end products (AGEs) as well as oxidative DNA damage were reported. In this study, we investigated the protective effect of cyanidin against MG-induced oxidative stress and apoptosis in rat INS-1 pancreatic β-cells. Exposure of cells to cytotoxic levels of MG (500 µM) for 12 h caused a significant reduction in cell viability. However, the pretreatment of cells with cyanidin alone (6.25–100 μM) for 12 h, or cotreatment of cells with cyanidin (3.13–100 μM) and MG, protected against cell cytotoxicity. In the cotreatment condition, cyanidin (33.3 and 100 μM) also decreased MG-induced apoptosis as determined by caspase-3 activity. Furthermore, INS-1 cells treated with MG increased the generation of reactive oxygen species (ROS) during a 6 h exposure. The MG-induced increase in ROS production was inhibited by cyanidin (33.3 and 100 μM) after 3 h stimulation. Furthermore, MG diminished the activity of glyoxalase 1 (Glo-1) and its gene expression as well as the level of total glutathione. In contrast, cyanidin reversed the inhibitory effect of MG on Glo-1 activity and glutathione levels. Interestingly, cyanidin alone was capable of increasing Glo-1 activity and glutathione levels without affecting Glo-1 mRNA expression. These findings suggest that cyanidin exerts a protective effect against MG-induced oxidative stress and apoptosis in pancreatic β-cells by increasing the activity of Glo-1.
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spelling pubmed-72847592020-06-15 Cyanidin Attenuates Methylglyoxal-Induced Oxidative Stress and Apoptosis in INS-1 Pancreatic β-Cells by Increasing Glyoxalase-1 Activity Suantawee, Tanyawan Thilavech, Thavaree Cheng, Henrique Adisakwattana, Sirichai Nutrients Article Recently, the mechanisms responsible for anti-glycation activity of cyanidin and its derivatives on the inhibition of methylglyoxal (MG)-induced protein glycation and advanced glycation-end products (AGEs) as well as oxidative DNA damage were reported. In this study, we investigated the protective effect of cyanidin against MG-induced oxidative stress and apoptosis in rat INS-1 pancreatic β-cells. Exposure of cells to cytotoxic levels of MG (500 µM) for 12 h caused a significant reduction in cell viability. However, the pretreatment of cells with cyanidin alone (6.25–100 μM) for 12 h, or cotreatment of cells with cyanidin (3.13–100 μM) and MG, protected against cell cytotoxicity. In the cotreatment condition, cyanidin (33.3 and 100 μM) also decreased MG-induced apoptosis as determined by caspase-3 activity. Furthermore, INS-1 cells treated with MG increased the generation of reactive oxygen species (ROS) during a 6 h exposure. The MG-induced increase in ROS production was inhibited by cyanidin (33.3 and 100 μM) after 3 h stimulation. Furthermore, MG diminished the activity of glyoxalase 1 (Glo-1) and its gene expression as well as the level of total glutathione. In contrast, cyanidin reversed the inhibitory effect of MG on Glo-1 activity and glutathione levels. Interestingly, cyanidin alone was capable of increasing Glo-1 activity and glutathione levels without affecting Glo-1 mRNA expression. These findings suggest that cyanidin exerts a protective effect against MG-induced oxidative stress and apoptosis in pancreatic β-cells by increasing the activity of Glo-1. MDPI 2020-05-06 /pmc/articles/PMC7284759/ /pubmed/32384625 http://dx.doi.org/10.3390/nu12051319 Text en © 2020 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
Suantawee, Tanyawan
Thilavech, Thavaree
Cheng, Henrique
Adisakwattana, Sirichai
Cyanidin Attenuates Methylglyoxal-Induced Oxidative Stress and Apoptosis in INS-1 Pancreatic β-Cells by Increasing Glyoxalase-1 Activity
title Cyanidin Attenuates Methylglyoxal-Induced Oxidative Stress and Apoptosis in INS-1 Pancreatic β-Cells by Increasing Glyoxalase-1 Activity
title_full Cyanidin Attenuates Methylglyoxal-Induced Oxidative Stress and Apoptosis in INS-1 Pancreatic β-Cells by Increasing Glyoxalase-1 Activity
title_fullStr Cyanidin Attenuates Methylglyoxal-Induced Oxidative Stress and Apoptosis in INS-1 Pancreatic β-Cells by Increasing Glyoxalase-1 Activity
title_full_unstemmed Cyanidin Attenuates Methylglyoxal-Induced Oxidative Stress and Apoptosis in INS-1 Pancreatic β-Cells by Increasing Glyoxalase-1 Activity
title_short Cyanidin Attenuates Methylglyoxal-Induced Oxidative Stress and Apoptosis in INS-1 Pancreatic β-Cells by Increasing Glyoxalase-1 Activity
title_sort cyanidin attenuates methylglyoxal-induced oxidative stress and apoptosis in ins-1 pancreatic β-cells by increasing glyoxalase-1 activity
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7284759/
https://www.ncbi.nlm.nih.gov/pubmed/32384625
http://dx.doi.org/10.3390/nu12051319
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