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In Silico Evaluation of the Potential Antiarrhythmic Effect of Epigallocatechin-3-Gallate on Cardiac Channelopathies
Ion channels are transmembrane proteins that allow the passage of ions according to the direction of their electrochemical gradients. Mutations in more than 30 genes encoding ion channels have been associated with an increasingly wide range of inherited cardiac arrhythmias. In this line, ion channel...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi Publishing Corporation
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5110949/ https://www.ncbi.nlm.nih.gov/pubmed/27882075 http://dx.doi.org/10.1155/2016/7861653 |
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author | Boukhabza, Maroua El Hilaly, Jaouad Attiya, Nourdine El-Haidani, Ahmed Filali-Zegzouti, Younes Mazouzi, Driss Amarouch, Mohamed-Yassine |
author_facet | Boukhabza, Maroua El Hilaly, Jaouad Attiya, Nourdine El-Haidani, Ahmed Filali-Zegzouti, Younes Mazouzi, Driss Amarouch, Mohamed-Yassine |
author_sort | Boukhabza, Maroua |
collection | PubMed |
description | Ion channels are transmembrane proteins that allow the passage of ions according to the direction of their electrochemical gradients. Mutations in more than 30 genes encoding ion channels have been associated with an increasingly wide range of inherited cardiac arrhythmias. In this line, ion channels become one of the most important molecular targets for several classes of drugs, including antiarrhythmics. Nevertheless, antiarrhythmic drugs are usually accompanied by some serious side effects. Thus, developing new approaches could offer added values to prevent and treat the episodes of arrhythmia. In this sense, green tea catechins seem to be a promising alternative because of the significant effect of Epigallocatechin-3-Gallate (E3G) on the electrocardiographic wave forms of guinea pig hearts. Thus, the aim of this study was to evaluate the benefits-risks balance of E3G consumption in the setting of ion channel mutations linked with aberrant cardiac excitability phenotypes. Two gain-of-function mutations, Na(v1.5)-p.R222Q and Na(v1.5)-p.I141V, which are linked with cardiac hyperexcitability phenotypes were studied. Computer simulations of action potentials (APs) show that 30 μM E3G reduces and suppresses AP abnormalities characteristics of these phenotypes. These results suggest that E3G may have a beneficial effect in the setting of cardiac sodium channelopathies displaying a hyperexcitability phenotype. |
format | Online Article Text |
id | pubmed-5110949 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-51109492016-11-23 In Silico Evaluation of the Potential Antiarrhythmic Effect of Epigallocatechin-3-Gallate on Cardiac Channelopathies Boukhabza, Maroua El Hilaly, Jaouad Attiya, Nourdine El-Haidani, Ahmed Filali-Zegzouti, Younes Mazouzi, Driss Amarouch, Mohamed-Yassine Comput Math Methods Med Research Article Ion channels are transmembrane proteins that allow the passage of ions according to the direction of their electrochemical gradients. Mutations in more than 30 genes encoding ion channels have been associated with an increasingly wide range of inherited cardiac arrhythmias. In this line, ion channels become one of the most important molecular targets for several classes of drugs, including antiarrhythmics. Nevertheless, antiarrhythmic drugs are usually accompanied by some serious side effects. Thus, developing new approaches could offer added values to prevent and treat the episodes of arrhythmia. In this sense, green tea catechins seem to be a promising alternative because of the significant effect of Epigallocatechin-3-Gallate (E3G) on the electrocardiographic wave forms of guinea pig hearts. Thus, the aim of this study was to evaluate the benefits-risks balance of E3G consumption in the setting of ion channel mutations linked with aberrant cardiac excitability phenotypes. Two gain-of-function mutations, Na(v1.5)-p.R222Q and Na(v1.5)-p.I141V, which are linked with cardiac hyperexcitability phenotypes were studied. Computer simulations of action potentials (APs) show that 30 μM E3G reduces and suppresses AP abnormalities characteristics of these phenotypes. These results suggest that E3G may have a beneficial effect in the setting of cardiac sodium channelopathies displaying a hyperexcitability phenotype. Hindawi Publishing Corporation 2016 2016-11-02 /pmc/articles/PMC5110949/ /pubmed/27882075 http://dx.doi.org/10.1155/2016/7861653 Text en Copyright © 2016 Maroua Boukhabza et al. https://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Boukhabza, Maroua El Hilaly, Jaouad Attiya, Nourdine El-Haidani, Ahmed Filali-Zegzouti, Younes Mazouzi, Driss Amarouch, Mohamed-Yassine In Silico Evaluation of the Potential Antiarrhythmic Effect of Epigallocatechin-3-Gallate on Cardiac Channelopathies |
title |
In Silico Evaluation of the Potential Antiarrhythmic Effect of Epigallocatechin-3-Gallate on Cardiac Channelopathies |
title_full |
In Silico Evaluation of the Potential Antiarrhythmic Effect of Epigallocatechin-3-Gallate on Cardiac Channelopathies |
title_fullStr |
In Silico Evaluation of the Potential Antiarrhythmic Effect of Epigallocatechin-3-Gallate on Cardiac Channelopathies |
title_full_unstemmed |
In Silico Evaluation of the Potential Antiarrhythmic Effect of Epigallocatechin-3-Gallate on Cardiac Channelopathies |
title_short |
In Silico Evaluation of the Potential Antiarrhythmic Effect of Epigallocatechin-3-Gallate on Cardiac Channelopathies |
title_sort | in silico evaluation of the potential antiarrhythmic effect of epigallocatechin-3-gallate on cardiac channelopathies |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5110949/ https://www.ncbi.nlm.nih.gov/pubmed/27882075 http://dx.doi.org/10.1155/2016/7861653 |
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