Evaluation of the Potential Antiarrhythmic Effect of Epigallocatechin-3-Gallate on Cardiac Channelopathies.

Comput Math Methods Med

Materials, Natural Substances, Environment and Modeling Laboratory, Multidisciplinary Faculty of Taza, University Sidi Mohamed Ben Abdellah, Fez, Morocco; Biology, Environment & Health Team, Department of Biology, Faculty of Sciences and Techniques Errachidia, University of Moulay Ismaïl, Meknes, Morocco.

Published: March 2017

AI Article Synopsis

  • Ion channels are proteins that facilitate ion movement across cell membranes, and mutations in these channels can lead to inherited heart rhythm disorders.
  • Many antiarrhythmic drugs target these channels but often come with serious side effects, prompting the search for safer alternatives.
  • This study found that Epigallocatechin-3-Gallate (E3G), from green tea, may reduce abnormalities in heart activity caused by specific ion channel mutations associated with heightened cardiac excitability.

Article Abstract

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-p.R222Q and Na-p.I141V, which are linked with cardiac hyperexcitability phenotypes were studied. Computer simulations of action potentials (APs) show that 30 M 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.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5110949PMC
http://dx.doi.org/10.1155/2016/7861653DOI Listing

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