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Permanent link (DOI): https://doi.org/10.7939/R3ZK6P

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Docosahexaenoic Acid Induced Apoptosis In H9c2 Cells And Changed Cardiac Function After Ischemia-Reperfusion Injury Open Access

Descriptions

Other title
Subject/Keyword
H9c2 cells
Apoptosis
DHA
Ischemia/reperfusion injury
Type of item
Thesis
Degree grantor
University of Alberta
Author or creator
Qadhi, Rawabi
Supervisor and department
Seubert, John (Pharmaceutical Sciences)
Examining committee member and department
El-Kadi, Ayman (Pharmaceutical Sciences)
Lavasanifar, Afsaneh (Pharmaceutical Sciences)
Davidge, Sandra (Obstetrics/Gynecology and Physiology)
Department
Faculty of Pharmacy and Pharmaceutical Sciences
Specialization
Pharmaceutical Sciences
Date accepted
2013-01-30T08:50:41Z
Graduation date
2013-06
Degree
Master of Science
Degree level
Master's
Abstract
Cardiovascular disease (CVD) remains one of the leading causes of death worldwide. As such, a vast amount of research has investigated novel therapies for preventing and/or reducing CVD. Much evidence has demonstrated the importance of dietary composition in increasing or lowering risks of CVD. While the role played by dietary n-3 polyunsaturated fatty acids (PUFAs) in reducing CVD has been recognized for many years, the protective mechanisms of these molecules, notably toward ischemia-reperfusion (IR) injury, remain unknown. Ecosapentaenoic acid (20:5n-3) and docosahexaenoic acid (22:6n-3, DHA) are two of the most important n-3 PUFAs. Both are present in fish oil. The objective of this study is to investigate the effect of acute administration of DHA on IR injury. Methods: Hearts from male C57BL6 mice were isolated and perfused in Langendorff mode and then subjected to IR injury. Hearts were perfused with different concentrations of DHA (0, 10, 50 and 100 µM) to determine its effect on cardiac function and recovery. Mechanistic studies were performed using rat myoblast cells (H9c2 cells) in an anoxia-reoxygenation protocol. Cell viability (MTT assay), cytochrome c release, and caspase-3 and caspase-8 activities were measured to compare cellular injury in DHA treated cells versus controls. The impact of DHA on mitochondrial morphology and function was assessed using epifluorescent microscopy. Results: Data demonstrated that DHA has adverse effects on both pre- and post-ischemic left ventricular developed pressures and on the heart rate, systolic and diastolic heart rates. Cell experiments revealed that significant cell death occurs in a concentration-dependent manner when H9c2 cells are treated with DHA and subjected to anoxia-reoxygenation injury. Moreover, apoptotic cell death is caused by DHA treatment, during which cytochrome c is released and caspases-8 and -3 are activated. Significant mitochondrial fragmentation and loss of membrane potential were observed with high concentrations of DHA. Conclusion: Our data suggest that acute treatment with DHA impedes the function of isolated hearts and triggers apoptotic cell death.
Language
English
DOI
doi:10.7939/R3ZK6P
Rights
Permission is hereby granted to the University of Alberta Libraries to reproduce single copies of this thesis and to lend or sell such copies for private, scholarly or scientific research purposes only. Where the thesis is converted to, or otherwise made available in digital form, the University of Alberta will advise potential users of the thesis of these terms. The author reserves all other publication and other rights in association with the copyright in the thesis and, except as herein before provided, neither the thesis nor any substantial portion thereof may be printed or otherwise reproduced in any material form whatsoever without the author's prior written permission.
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