The Efficacy of Etoposide on H9c2 Cardiomyoblasts Against Doxorubicin Induced Cardiotoxicity
Author | Shabana, Sara |
Author | Aden, Suad |
Author | Abdulrahman, Nabeel |
Author | Riaz, Sadaf |
Author | Jaballah, Maiy |
Author | Mohamed, Iman A. |
Author | Mraiche, Fatima |
Available date | 2017-04-05T10:55:51Z |
Publication Date | 2015 |
Publication Name | Anatomy & Physiology: Current Research |
Identifier | http://dx.doi.org/10.4172/2161-0940.1000186 |
Citation | Shabana S, Aden S, Abdulrahman N, Riaz S, Jaballah M, et al. (2015) The Efficacy of Etoposide on H9c2 Cardiomyoblasts Against Doxorubicin Induced Cardiotoxicity. Anat Physiol 5:186. doi: 10.4172/2161-0940.1000186 |
ISSN | 2161-0940 |
Abstract | Background: Doxorubicin (DOX), a widely used anticancer drug, has been associated with cardiotoxicity. Recently, DOX-induced cardiotoxicity has been attributed to topoisomerase II (TOPII)-β expression and activity. In our study, we investigated the effect of inhibiting TOPII in attenuating the DOX induced cardiotoxicity. Method: H9c2 cardiomyoblasts were treated with 1 or 2 µM DOX (+/-) 1 µM ETO. Cardiotoxicity was assessed by examining cell viability using the MTT assay, hypertrophy of crystal violet stained cardiomyoblasts and ROS production. Results: DOX induced a dose dependent increase in cardiotoxicity as indicated by the significant reduction in cell viability (71.77 ± 9.25% 2 µM DOX vs. 100% control, P<0.05), ROS production and hypertrophy. Stimulation of H9c2 cardiomyoblasts with both 2 µM DOX and 1µM ETO did not show a significant difference in cell viability, ROS production or hypertrophy. Conclusion: DOX induced cardiotoxicity in H9c2 cardiomyoblasts was not exacerbated in the presence of 1 µM ETO. This provides further support to using the combination |
Language | en |
Publisher | OMICS International |
Subject | Doxorubicin Etoposide Topoisomerase Cardiomyocyte hypertrophy |
Type | Article |
Issue Number | 4 |
Volume Number | 5 |
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