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 ROSproduction. 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 of DOX and ETO, which is currently being done to treat advanced AIDS related sarcomas in the clinical setting.
Highlights
Doxorubicin (DOX), one of the most effective and used anthracyclines [1], has been used for several decades due to its potent broads spectrum antineoplastic activity [2]
Stimulation of H9c2 cardiomyoblasts with both 2 μM DOX and 1μM ETO did not show a significant difference in cell viability, reactive oxygen species (ROS) production or hypertrophy
DOX induced cardiotoxicity in H9c2 cardiomyoblasts was not exacerbated in the presence of 1 μM ETO
Summary
Doxorubicin (DOX), one of the most effective and used anthracyclines [1], has been used for several decades due to its potent broads spectrum antineoplastic activity [2]. Despite the clinical application of DOX, it is well known to induce a dose-dependent cardiotoxicity, which limits its clinical usage [7]. DOX induced cardiotoxicity, early-onset or late onset, is characterized by a decline in left ventricular ejection fraction or the development of congestive heart failure [1]. Doxorubicin (DOX), a widely used anticancer drug, has been associated with cardiotoxicity. DOX-induced cardiotoxicity has been attributed to topoisomerase II (TOPII)-β expression and activity. We investigated the effect of inhibiting TOPII in attenuating the DOX induced cardiotoxicity
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