Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 홍영미 | * |
dc.contributor.author | 조민선 | * |
dc.contributor.author | 김관창 | * |
dc.date.accessioned | 2017-12-28T16:30:20Z | - |
dc.date.available | 2017-12-28T16:30:20Z | - |
dc.date.issued | 2017 | * |
dc.identifier.issn | 1738-1061 | * |
dc.identifier.other | OAK-21765 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/239522 | - |
dc.description.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. © 2017 by The Korean Pediatric Society. | * |
dc.language | English | * |
dc.publisher | Korean Pediatric Society | * |
dc.subject | Apoptosis | * |
dc.subject | Cardiomyopathies | * |
dc.subject | Doxorubicin | * |
dc.subject | Ventricular remodeling | * |
dc.title | Apoptosis and remodeling in adriamycin-induced cardiomyopathy rat model | * |
dc.type | Article | * |
dc.relation.issue | 11 | * |
dc.relation.volume | 60 | * |
dc.relation.index | SCOPUS | * |
dc.relation.index | KCI | * |
dc.relation.startpage | 365 | * |
dc.relation.lastpage | 372 | * |
dc.relation.journaltitle | Korean Journal of Pediatrics | * |
dc.identifier.doi | 10.3345/kjp.2017.60.11.365 | * |
dc.identifier.scopusid | 2-s2.0-85035003483 | * |
dc.author.google | Hong Y.M. | * |
dc.author.google | Lee H. | * |
dc.author.google | Cho M.-S. | * |
dc.author.google | Kim K.C. | * |
dc.contributor.scopusid | 홍영미(35210025100;55841904000;56063366100) | * |
dc.contributor.scopusid | 조민선(13205279200) | * |
dc.contributor.scopusid | 김관창(36652690000) | * |
dc.date.modifydate | 20240415130647 | * |