The Efficacy of Etoposide on H9c2 Cardiomyoblasts Against Doxorubicin Induced Cardiotoxicity

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