Key result
Resveratrol and FGF1 co-treatment reduces doxorubicin-induced cardiotoxicity and limits FGF1 growth-promoting activity.
Why the study?
DOX causes dose-dependent cardiotoxicity, while cardioprotective native FGF1 carries tumorigenic risk and anti-proliferative RES may serve as an auxiliary therapy.
Does co-treatment with resveratrol and FGF1 reduce doxorubicin-induced cardiotoxicity in preclinical models?
Does co-treatment with resveratrol and FGF1 reduce doxorubicin-induced cardiotoxicity in preclinical models?
Co-treatment with resveratrol and FGF1 synergistically protects against doxorubicin-induced cardiotoxicity while mitigating the tumorigenic risk of FGF1 in preclinical models.
Does not support clinical use; hypothesis-generating for doxorubicin cardiotoxicity in animal models.
Doxorubicin (DOX) has received attention due to dose-dependent cardiotoxicity through abnormal redox cycling. Native fibroblast growth factor 1 (FGF1) is known for its anti-oxidative benefits in cardiovascular diseases, but possesses a potential tumorigenic risk. Coincidentally, the anti-proliferative properties of resveratrol (RES) have attracted attention as alternatives or auxiliary therapy when combined with other chemotherapeutic drugs. Therefore, the purpose of this study is to explore the therapeutic potential and underlying mechanisms of co-treatment of RES and FGF1 in a DOX-treated model. Here, various cancer cells were applied to determine whether RES could antagonize the oncogenesis effect of FGF1. In addition, C57BL/6J mice and H9c2 cells were used to testify the therapeutic potential of a co-treatment of RES and FGF1 against DOX-induced cardiotoxicity. We found RES could reduce the growth-promoting activity of FGF1. Additionally, the co-treatment of RES and FGF1 exhibits a more powerful cardio-antioxidative capacity in a DOX-treated model. The inhibition of SIRT1/NRF2 abolished RES in combination with FGF1 on cardioprotective action. Further mechanism analysis demonstrated that SIRT1 and NRF2 might form a positive feedback loop to perform the protective effect on DOX-induced cardiotoxicity. These favorable anti-oxidative activities and reduced proliferative properties of the co-treatment of RES and FGF1 provided a promising therapy for anthracycline cardiotoxicity during chemotherapy.
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Lu et al. (2022) studied Doxorubicin-induced cardiotoxicity. Co-treatment of resveratrol (RES) and FGF1 was evaluated on Cardio-antioxidative capacity and DOX-induced cardiotoxicity. Co-treatment of resveratrol and FGF1 reduced the growth-promoting activity of FGF1 and exhibited powerful cardio-antioxidative capacity against doxorubicin-induced cardiotoxicity.
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