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Probucol prevents atrial ion channel remodeling in an alloxan-induced diabetes rabbit model
Diabetes mellitus (DM) increases the risk of developing atrial fibrillation (AF), but the molecular mechanisms of diabetes-induced atrial remodeling processes have not been fully characterized. The aim of this study was to examine the mechanisms underlying atrial ion channel remodeling in alloxan-in...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Impact Journals LLC
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5356629/ https://www.ncbi.nlm.nih.gov/pubmed/27863381 http://dx.doi.org/10.18632/oncotarget.13339 |
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author | Fu, Huaying Li, Guangping Liu, Changle Li, Jian Cheng, Lijun Yang, Wansong Tse, Gary Zhao, Jichao Liu, Tong |
author_facet | Fu, Huaying Li, Guangping Liu, Changle Li, Jian Cheng, Lijun Yang, Wansong Tse, Gary Zhao, Jichao Liu, Tong |
author_sort | Fu, Huaying |
collection | PubMed |
description | Diabetes mellitus (DM) increases the risk of developing atrial fibrillation (AF), but the molecular mechanisms of diabetes-induced atrial remodeling processes have not been fully characterized. The aim of this study was to examine the mechanisms underlying atrial ion channel remodeling in alloxan-induced diabetes model in rabbits. A total of 40 Japanese rabbits were randomly assigned to a control group (C), alloxan-induced diabetic group (DM), probucol-treated control group (Control-P), and probucol-treated diabetic group (DM-P). Using whole-cell voltage-clamp techniques, I(Ca,L), I(Na) and action potential durations (APDs) were measured in cardiomyocytes isolated from the left atria in the four groups, respectively. In the DM group, increased I(ca,L) and decreased I(Na) currents were reflected in prolonged APD(90) and APD(50) values. These changes were reversed in the DM-P group. In conclusion, probucol cured AF by alleviating the ion channel remodeling of atrial myocytes in the setting of diabetes and the promising therapeutic potential of anti-oxidative compounds in the treatment of AF warrants further study. |
format | Online Article Text |
id | pubmed-5356629 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Impact Journals LLC |
record_format | MEDLINE/PubMed |
spelling | pubmed-53566292017-04-26 Probucol prevents atrial ion channel remodeling in an alloxan-induced diabetes rabbit model Fu, Huaying Li, Guangping Liu, Changle Li, Jian Cheng, Lijun Yang, Wansong Tse, Gary Zhao, Jichao Liu, Tong Oncotarget Research Paper: Pathology Diabetes mellitus (DM) increases the risk of developing atrial fibrillation (AF), but the molecular mechanisms of diabetes-induced atrial remodeling processes have not been fully characterized. The aim of this study was to examine the mechanisms underlying atrial ion channel remodeling in alloxan-induced diabetes model in rabbits. A total of 40 Japanese rabbits were randomly assigned to a control group (C), alloxan-induced diabetic group (DM), probucol-treated control group (Control-P), and probucol-treated diabetic group (DM-P). Using whole-cell voltage-clamp techniques, I(Ca,L), I(Na) and action potential durations (APDs) were measured in cardiomyocytes isolated from the left atria in the four groups, respectively. In the DM group, increased I(ca,L) and decreased I(Na) currents were reflected in prolonged APD(90) and APD(50) values. These changes were reversed in the DM-P group. In conclusion, probucol cured AF by alleviating the ion channel remodeling of atrial myocytes in the setting of diabetes and the promising therapeutic potential of anti-oxidative compounds in the treatment of AF warrants further study. Impact Journals LLC 2016-11-14 /pmc/articles/PMC5356629/ /pubmed/27863381 http://dx.doi.org/10.18632/oncotarget.13339 Text en Copyright: © 2016 Fu et al. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Paper: Pathology Fu, Huaying Li, Guangping Liu, Changle Li, Jian Cheng, Lijun Yang, Wansong Tse, Gary Zhao, Jichao Liu, Tong Probucol prevents atrial ion channel remodeling in an alloxan-induced diabetes rabbit model |
title | Probucol prevents atrial ion channel remodeling in an alloxan-induced diabetes rabbit model |
title_full | Probucol prevents atrial ion channel remodeling in an alloxan-induced diabetes rabbit model |
title_fullStr | Probucol prevents atrial ion channel remodeling in an alloxan-induced diabetes rabbit model |
title_full_unstemmed | Probucol prevents atrial ion channel remodeling in an alloxan-induced diabetes rabbit model |
title_short | Probucol prevents atrial ion channel remodeling in an alloxan-induced diabetes rabbit model |
title_sort | probucol prevents atrial ion channel remodeling in an alloxan-induced diabetes rabbit model |
topic | Research Paper: Pathology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5356629/ https://www.ncbi.nlm.nih.gov/pubmed/27863381 http://dx.doi.org/10.18632/oncotarget.13339 |
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