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Investigation of the impact of rosuvastatin and telmisartan in doxorubicin-induced acute cardiotoxicity

Cardiac injury is the main dose-limiting factor for doxorubicin (Dox) use as an anticancer agent. The cardiotoxicity of Dox is linked to a number of complex mechanisms, including oxidative stress, mitochondrial damage, intracellular calcium dysregulation, and apoptosis/necrosis. This study investigates several aspects of Dox-induced cardiotoxicity. We investigated the effects of pre-treatment with rosuvastatin and telmisartan, which were used in different doses alone or combination, on the acute cardiotoxicity induced by Dox. The results of this study showed that Dox induced significant pathological changes in the cardiomyocytes. Adverse effects were observed on several biomarkers related to cardiac damage like cardiac troponin I (cTnI) and lactate dehydrogenase (LDH), oxidative stress like malondialdehyde (MDA), an inflammatory process like interleukin-17 (IL-17) with important histopathological changes. We illusterate the cardio-protective contribution of the two pharmacological agents against the acute cardiotoxic effects of Dox. This is manifested by the significant improvement in the biomarker levels and the associated histological damage. This study points out the beneficial use of both rosuvastatin and telmisartan alone or in combination as a clinical option for decreasing the acute toxicity of Dox on cardiomyocytes.

 

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This study investigates the effects of pre-treatment with rosuvastatin and telmisartan, alone or in combination, on the acute cardiotoxicity induced by the anticancer agent doxorubicin (Dox). The cardiotoxicity of Dox is linked to oxidative stress, mitochondrial damage, intracellular calcium dysregulation, and apoptosis/necrosis. The study found that Dox induced significant pathological changes in cardiomyocytes and adversely affected several biomarkers related to cardiac damage, oxidative stress, and inflammation. However, pre-treatment with rosuvastatin and telmisartan showed a significant improvement in the biomarker levels and the associated histological damage, indicating the cardio-protective contribution of these pharmacological agents against the acute cardiotoxic effects of Dox. These findings suggest that both rosuvastatin and telmisartan, alone or in combination, could be a beneficial clinical option for decreasing the acute toxicity of Dox on cardiomyocytes.

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