Protective Effects of Quercetin, Curcumin and Resveratrol in an in Vitro Model of Doxorubicin-Induced Cardiotoxicity
B. Stoyanov
Profil Orcid, , oraz 
Data publikacji: 09 wrz 2025
Zakres stron: 53 - 62
Otrzymano: 14 sty 2025
Przyjęty: 09 maj 2025
DOI: https://doi.org/10.2478/amb-2025-00061
Słowa kluczowe
© 2025 B. Stoyanov et al., published by Sciendo
This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
Introduction
Over the past two decades, drug-induced cardiotoxicity has resulted in the withdrawal of several drugs, including prenylamine, rofecoxib, and levomethadyl acetate, while others like rosiglitazone remain available only under restricted conditions. However, some cardiotoxic drugs, like doxorubicin (DOX), are still used due to their potent antitumor activity despite their dose-dependent cardiotoxicity. This cardiotoxicity, often caused by lipid peroxidation and reactive oxygen species (ROS), can be mitigated by natural substances like quercetin (QR), curcumin (CRC), and resveratrol (RES), which have notable antioxidant and cardioprotective effects.
Aim
This study aimed to evaluate the potential of QR, RES, and CRC to enhance the viability of H9c2 cardiomyocytes in an in vitro model of doxorubicin-induced cardiotoxicity.
Materials and Methods
H9c2 cells were treated with doxorubicin (0.25 μM and 1 μM) and varying concentrations of QR, RES, and CRC (0.01 μM, 0.1 μM, 1 μM, 2.5 μM, 5 μM, 10 μM) for 24 and 48 h. Cell viability was assessed using the MTT assay to determine the protective effects of the natural antioxidants on H9c2 cell line.
Results
Our data demonstrated that QR and CRC significantly improved the viability of H9c2 cells in the DOX-induced cardiotoxicity model of treatment with 0.25 μM DOX (24 h). At these conditions, RES also showed protective cell viability effects, but it was not effective at the injury with higher DOX concentration (1 μM, 24 h).
Conclusions
This study highlights the in vitro protective effects of QR and CRC in reducing DOX-induced cardiotoxicity in H9c2 cardioblast cells, most probably attributed to their well-established antioxidant effects.