Apoptosis and remodeling in adriamycin-induced cardiomyopathy rat model.
10.3345/kjp.2017.60.11.365
- Author:
Young Mi HONG
1
;
Hyeryon LEE
;
Min Sun CHO
;
Kwan Chang KIM
Author Information
1. Department of Pediatrics, Ewha Womans University School of Medicine, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Doxorubicin;
Cardiomyopathies;
Apoptosis;
Ventricular remodeling
- MeSH:
Animals;
Apoptosis*;
Ascites;
B-Lymphocytes;
Blotting, Western;
Cardiomyopathies*;
Caspase 3;
Collagen;
Depression;
Doxorubicin;
Echocardiography;
Fibrosis;
Free Radicals;
Gene Expression;
Heart Failure;
Heart Ventricles;
Humans;
Hypertrophy, Left Ventricular;
Injections, Intraperitoneal;
Interleukin-6;
Interleukins;
Male;
Models, Animal*;
Natriuretic Peptide, Brain;
Necrosis;
Rats*;
Rats, Sprague-Dawley;
Troponin I;
Up-Regulation;
Ventricular Remodeling
- From:Korean Journal of Pediatrics
2017;60(11):365-372
- CountryRepublic of Korea
- Language:English
-
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.
