| Apoptosis and remodeling in adriamycin-induced cardiomyopathy rat model |
| Young Mi Hong1, Hyeryon Lee1, Min-Sun Cho2, Kwan Chang Kim3 |
1Department of Pediatrics, Ewha Womans University School of Medicine, Seoul, Korea
2Department of Pathology, Ewha Womans University School of Medicine, Seoul, Korea
3Department of Thoracic and Cardiovascular Surgery, Ewha Womans University School of Medicine, Seoul, Korea |
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Corresponding Author:
Kwan Chang Kim ,Tel: +82-2-2650-5151, Fax: +82-2-2650-5152, Email: mdkkchang@ewha.ac.kr |
| Copyright © 2017 by The Korean Pediatric Society |
| ABSTRACT |
Purpose: The mechanism for the pathogenesis of adriamycin (ADR)-induced cardiomyopathy is not yet known. Different hypotheses include the production of free radicals, an interaction between ADR and nuclear components, and a disruption in cardiac-specific gene expression. Apoptosis has also been proposed as being involved in cardiac dysfunction. The purpose of this study was to determine if apoptosis might play a role in ADR-induced cardiomyopathy.
Methods: Male Sprague-Dawley rats were separated into 2 groups: the control group (C group) and the experimental group (ADR 5 mg/wk for 3 weeks through intraperitoneal injections; A group). Echocardiographic images were obtained at week 3. Changes in caspase-3, B-cell leukemia/lymphoma (Bcl)-2, Bcl-2-associated X (Bax), interleukin (IL)-6, tumor necrosis factor-α, brain natriuretic peptide (BNP), troponin I, collagen 1, and collagen 3 protein expression from the left ventricle tissues of C and A group rats were determined by Western blot.
Results: Ascites and heart failure as well as left ventricular hypertrophy were noted in the A group. Ejection fraction and shortening fraction were significantly lower in the A group by echocardiography. The expression of caspase-3, Bax, IL-6, BNP, collagen 1, and collagen 3 were significantly higher in the A group as compared with the C group. Protein expression of Bcl-2 decreased significantly in the A group compared with the C group.
Conclusion: ADR induced an upregulation of caspase-3, Bax, IL-6, and collagen, as well as a depression in Bcl-2. Thus, apoptosis and fibrosis may play an important role in ADR-induced cardiomyopathy. |
| Keywords:
Doxorubicin | Cardiomyopathies | Apoptosis | Ventricular remodeling
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