Cancer ranks second in frequency among non-communicable diseases after cardiovascular disorders. The increased life expectancy has made cancers more common, making it crucial to avoid side effects of the medications used to treat them. SGLT2i medications lower the risk of significant cardiovascular events and heart failure-related hospitalizations, as shown in clinical trials. Dapagliflozin is one such medication that is primarily regulated by blood glucose levels but may also impact cardiac disorders through other processes. This study will evaluate the potential protective effects of Dapagliflozin on DOX-induced cardiotoxicity in female rats, manifested by changes in biochemical parameters in tissue and serum samples, histopathological differences, and compare their changes. Twenty-four rats were divided into three weight-based groups. The first group received saline, the second group received doxorubicin, and the third group received dapagliflozin for three days before receiving doxorubicin for two weeks. Doxorubicin causes cardiotoxicity, as evidenced by increased caspase-3 and inflammatory markers. Dapagliflozin reduces cardiotoxicity by increasing SOD and GSH and decreasing caspase 3, as well as improving the CMYO score and lesions. Dapagliflozin successfully mitigated DOX-induced cardiotoxicity in rats at the concentrations utilized in this investigation. This phenomenon potentially pertains to inhibiting and safeguarding against oxidative stress, the pathway of apoptosis, and the inflammatory response.
