Abstract
Objective: In this study, the embryonic rat cardiomyocyte cell line H9C2 was used to investigate the cardiotoxicity effect of sappan wood ethanol extract (SWEE).
 Methods: Sappan wood was extracted in 96% ethanol and divided into dose concentrations of 2.5, 5, 10, 50, 100, and 150 μg/ml, with deferiprone used as a control. Cell viability was assessed using the PrestoBlue Cell Viability Reagent, according to manufacturer protocols.
 Results: Microscopic examination showed that the cell viability of H9C2 was preserved by SWEE treatments at a dose of 10 μg/ml and suggested dose concentrations of 50 μg/ml of SWEE. The percentage of viable cells was greater than 95% with a dose concentration of 10 μg/ml of SWEE, but it was significantly reduced with a dose concentration of 50 μg/ml of SWEE (p<0.05).
 Conclusion: The optimal dose concentration of SWEE to reach 95% cell viability was 10 μg/ml.
Highlights
Blood transfusion plays an important therapeutic role in patients with a history of diseases such as β-thalassemia, anemia, and myelodysplastic syndromes (MDS) [1,2,3]
The dried extract of Sappan wood was dissolved in dimethyl sulfoxide (DMSO) for further testing
A cytotoxic examination of sappan wood ethanol extract (SWEE) with concentrated variants of the H9C2 cell line showed a change of color after the PrestoBlue reagent was applied: the cell line turned purple and pink on several wells
Summary
Blood transfusion plays an important therapeutic role in patients with a history of diseases such as β-thalassemia, anemia, and myelodysplastic syndromes (MDS) [1,2,3]. Blood transfusion therapy has the risk of long-term side effects, causing an iron overload, where excess iron in the body accumulates in several organs, such as the liver, endocrine system, and heart. Excessive iron accumulation in the heart causes cardiomyopathy, a disease which can lead to heart failure [1]. When iron levels exceed the capacity limit of ferritin, cell death and organ damage will occur due to the presence of ROS and their consequent mutations [5]. Based on this reaction, it is clear that iron chelation is needed to control the amount of iron in the body, especially in iron overload conditions
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