ISSN: 2161-0940
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Sara Shabana, Suad Aden, Nabeel Abdulrahman, Sadaf Riaz, Maiy Jaballah, Iman A. Mohamed and Fatima Mraiche
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.
Published Date: 2020-12-31; Received Date: 2020-12-10