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

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 benef...

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Autores principales: González-Pacheco, Héctor, Méndez-Domínguez, Aurelio, Hernández, Salomón, López-Marure, Rebeca, Vazquez-Mellado, Maria J., Aguilar, Cecilia, Rocha-Zavaleta, Leticia
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3918843/
https://www.ncbi.nlm.nih.gov/pubmed/24578622
http://dx.doi.org/10.1155/2014/187071
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author González-Pacheco, Héctor
Méndez-Domínguez, Aurelio
Hernández, Salomón
López-Marure, Rebeca
Vazquez-Mellado, Maria J.
Aguilar, Cecilia
Rocha-Zavaleta, Leticia
author_facet González-Pacheco, Héctor
Méndez-Domínguez, Aurelio
Hernández, Salomón
López-Marure, Rebeca
Vazquez-Mellado, Maria J.
Aguilar, Cecilia
Rocha-Zavaleta, Leticia
author_sort González-Pacheco, Héctor
collection PubMed
description 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 H(2)O(2) 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.
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spelling pubmed-39188432014-02-26 Pre-Conditioning with CDP-Choline Attenuates Oxidative Stress-Induced Cardiac Myocyte Death in a Hypoxia/Reperfusion Model González-Pacheco, Héctor Méndez-Domínguez, Aurelio Hernández, Salomón López-Marure, Rebeca Vazquez-Mellado, Maria J. Aguilar, Cecilia Rocha-Zavaleta, Leticia ScientificWorldJournal Research Article 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 H(2)O(2) 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. Hindawi Publishing Corporation 2014-01-21 /pmc/articles/PMC3918843/ /pubmed/24578622 http://dx.doi.org/10.1155/2014/187071 Text en Copyright © 2014 Héctor González-Pacheco et al. https://creativecommons.org/licenses/by/3.0/ 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
González-Pacheco, Héctor
Méndez-Domínguez, Aurelio
Hernández, Salomón
López-Marure, Rebeca
Vazquez-Mellado, Maria J.
Aguilar, Cecilia
Rocha-Zavaleta, Leticia
Pre-Conditioning with CDP-Choline Attenuates Oxidative Stress-Induced Cardiac Myocyte Death in a Hypoxia/Reperfusion Model
title Pre-Conditioning with CDP-Choline Attenuates Oxidative Stress-Induced Cardiac Myocyte Death in a Hypoxia/Reperfusion Model
title_full Pre-Conditioning with CDP-Choline Attenuates Oxidative Stress-Induced Cardiac Myocyte Death in a Hypoxia/Reperfusion Model
title_fullStr Pre-Conditioning with CDP-Choline Attenuates Oxidative Stress-Induced Cardiac Myocyte Death in a Hypoxia/Reperfusion Model
title_full_unstemmed Pre-Conditioning with CDP-Choline Attenuates Oxidative Stress-Induced Cardiac Myocyte Death in a Hypoxia/Reperfusion Model
title_short Pre-Conditioning with CDP-Choline Attenuates Oxidative Stress-Induced Cardiac Myocyte Death in a Hypoxia/Reperfusion Model
title_sort pre-conditioning with cdp-choline attenuates oxidative stress-induced cardiac myocyte death in a hypoxia/reperfusion model
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3918843/
https://www.ncbi.nlm.nih.gov/pubmed/24578622
http://dx.doi.org/10.1155/2014/187071
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