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Apoptosis and remodeling in adriamycin-induced cardiomyopathy rat model
- Apoptosis and remodeling in adriamycin-induced cardiomyopathy rat model
- Hong Y.M.; Lee H.; Cho M.-S.; Kim K.C.
- Ewha Authors
- 홍영미; 조민선; 김관창
- SCOPUS Author ID
- 홍영미; 조민선; 김관창
- Issue Date
- Journal Title
- Korean Journal of Pediatrics
- vol. 60, no. 11, pp. 365 - 372
- Apoptosis; Cardiomyopathies; Doxorubicin; Ventricular remodeling
- Korean Pediatric Society
- SCOPUS; KCI
- 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. © 2017 by The Korean Pediatric Society.
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