RESEARCH ARTICLE
Protective Effect of 6-Gingerol Against Cardiotoxicity Induced by Doxorubicin
Mahmoud A. Mansour*, Saleh A. Bakheet, Abdulaziz M. Aleisa, Salim S. Al-Rejaie, Abdulaziz A. AL-Yahya, Mubarak El-Ameen , Othman A. Al-Shabanah
Article Information
Identifiers and Pagination:
Year: 2008Volume: 2
First Page: 20
Last Page: 23
Publisher Id: TOPHARMJ-2-20
DOI: 10.2174/1874143600802010020
Article History:
Received Date: 3/3/2008Revision Received Date: 12/3/2008
Acceptance Date: 18/3/2008
Electronic publication date: 27/3/2008
Collection year: 2008
open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: https://creativecommons.org/licenses/by/4.0/legalcode. This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Doxorubicin (DOX) has a wide spectrum of antitumor activity with dose-related cardiotoxicity as a major side effect. This cardiotoxicity has been suggested to result from enhanced oxidative stress caused by oxygen centered free radicals. The present study was performed to investigate the influence of the antioxidant 6-gingerol on cardiotoxicity induced by doxorubicin (DOX). A single dose of DOX (20 mg/kg i.p.) induced myocardial toxicity after 48 hrs, manifested biochemically by a significant elevation in the following serum enzymes activities: creatine phosphokinase (E.C.2.7.3.2), lactate dehydrogenase (E.C.1.1.1.27), aspartate transaminase (E.C.2.6.1.1) and serum cardiac isoenzyme creatine phosphokinase (MB). Administration of 6-gingerol (10 mg/kg/day p.o.) in drinking water starting 5 days before and continuing during the experimental period significantly ameliorated myocardial toxicity induced by DOX. The amelioration of cardiotoxicity was evidenced by significant reductions in serum enzymes activities and cardiac isoenzyme. The current data support 6-gingerol as a potentially selective cardioprotective agent, against cardiotoxicity induced by DOX and it may therefore improve the therapeutic index of DOX.
