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Apoptosis and remodeling in adriamycin-induced cardiomyopathy rat model
Young Mi Hong1, Hyeryon Lee1, Min-Sun Cho2
1Department of Pediatrics, Ewha Womans University School of Medicine, Seoul, Korea.
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.
Insights
Adriamycin (ADR) causes heart failure by increasing apoptosis and fibrosis. This study shows ADR upregulates caspase-3, Bax, IL-6, and collagen, while decreasing Bcl-2, confirming apoptosis
Area of Science:
- Cardiovascular Research
- Molecular Biology
- Toxicology
Background:
- The exact mechanism of adriamycin (ADR)-induced cardiomyopathy remains unclear.
- Hypotheses include free radical production, nuclear interactions, and altered gene expression.
- Apoptosis has been implicated in ADR-induced cardiac dysfunction.
Purpose of the Study:
- To investigate the role of apoptosis in adriamycin (ADR)-induced cardiomyopathy.
Main Methods:
- Male Sprague-Dawley rats received intraperitoneal injections of ADR (5 mg/wk for 3 weeks) or saline (control).
- Echocardiography was performed at week 3.
- Western blot analysis assessed protein expression of caspase-3, Bcl-2, Bax, IL-6, TNF-α, BNP, troponin I, collagen 1, and collagen 3 in left ventricle tissues.
Main Results:
- ADR-treated rats exhibited ascites, heart failure, and left ventricular hypertrophy.
- Echocardiography revealed significantly reduced ejection fraction and shortening fraction in the ADR group.
- ADR increased caspase-3, Bax, IL-6, BNP, collagen 1, and collagen 3 expression, while decreasing Bcl-2 expression compared to controls.
Conclusions:
- Adriamycin (ADR) induces apoptosis and fibrosis in the heart.
- Upregulation of caspase-3, Bax, IL-6, and collagen, alongside decreased Bcl-2, supports the role of apoptosis and fibrosis in ADR-induced cardiomyopathy.
