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The Scientific World Journal
Volume 2014, Article ID 187071, 8 pages
http://dx.doi.org/10.1155/2014/187071
Research Article

Pre-Conditioning with CDP-Choline Attenuates Oxidative Stress-Induced Cardiac Myocyte Death in a Hypoxia/Reperfusion Model

1Departamento de Urgencias y Unidad Coronaria, Instituto Nacional de Cardiología “Ignacio Chavez”, Juan Badiano No. 1, Colonia Seccion 16, 14080 Tlalpan, DF, Mexico
2Departamento de Neurologia, Instituto Nacional de Cardiología “Ignacio Chavez”, Juan Badiano No. 1, Colonia Seccion 16, 14080 Tlalpan, DF, Mexico
3Facultad de Medicina, Universidad Panamericana, Augusto Rodin 498, 03920 Insurgentes Mixcoac, DF, Mexico
4Departamento de Biologia Celular, Instituto Nacional de Cardiología “Ignacio Chavez”, Juan Badiano No. 1, Colonia Seccion 16, 14080 Tlalpan, DF, Mexico
5Departamento de Biología Molecular y Biotecnología, Instituto de Investigaciones Biomédicas, UNAM, Circuito Escolar s/n, Ciudad Universitaria, 04510 Coyoacan, DF, Mexico

Received 29 August 2013; Accepted 24 October 2013; Published 21 January 2014

Academic Editors: M. Karmazyn and R. M. Mentzer

Copyright © 2014 Héctor González-Pacheco et al. 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.

Abstract

Background. CDP-choline is a key intermediate in the biosynthesis of phosphatidylcholine, which is an essential component of cellular membranes, and a cell signalling mediator. CDP-choline has been used for the treatment of cerebral ischaemia, showing beneficial effects. However, its potential benefit for the treatment of myocardial ischaemia has not been explored yet. Aim. In the present work, we aimed to evaluate the potential use of CDP-choline as a cardioprotector in an in vitro model of ischaemia/reperfusion injury. Methods. Neonatal rat cardiac myocytes were isolated and subjected to hypoxia/reperfusion using the coverslip hypoxia model. To evaluate the effect of CDP-choline on oxidative stress-induced reperfusion injury, the cells were incubated with H2O2 during reperfusion. The effect of CDP-choline pre- and postconditioning was evaluated using the cell viability MTT assay, and the proportion of apoptotic and necrotic cells was analyzed using the Annexin V determination by flow cytometry. Results. Pre- and postconditioning with 50 mg/mL of CDP-choline induced a significant reduction of cells undergoing apoptosis after hypoxia/reperfusion. Preconditioning with CDP-choline attenuated postreperfusion cell death induced by oxidative stress. Conclusion. CDP-choline administration reduces cell apoptosis induced by oxidative stress after hypoxia/reperfusion of cardiac myocytes. Thus, it has a potential as cardioprotector in ischaemia/reperfusion-injured cardiomyocytes.