Objective: We aimed to test whether CBR1 inhibitor prevents heart failure cause by doxorubicin-induced cardiomyopathy in animal models and investigated the antitumor effect of doxorubicin in commonly used Breast cancer cells.
Methods and Results: Spra...
Objective: We aimed to test whether CBR1 inhibitor prevents heart failure cause by doxorubicin-induced cardiomyopathy in animal models and investigated the antitumor effect of doxorubicin in commonly used Breast cancer cells.
Methods and Results: Sprague-Dawley rats were divided into 4 groups: control, doxorubicin (2.5 mg/kg x 6 times IP), hydroxy-PP-Me (1.7 mg/kg x 6 times IP) and doxorubicin+ hydroxy-PP-Me. Doxorubicin-induced cardiotoxicity was attenuated by hydroxy-PP-Me as measured by echocardiogram and serum creatine phosphokinase activity. In breast cancer cells, Doxorubicin induced apoptosis increased by hydroxy-PP-Me as measured by cell viability, activated caspase-3, PARP cleavage, sub-G1 cell population and apoptotic morphology.
Conclusions: Doxorubicin, an anthracycline antibiotic, significantly improved anticancer agents potential by hydroxy-PP-Me in breast cancer cells and enhanced left ventricular function, hemodynamic parameters, myocardium morphology. Therefore, we concluded that hydroxy-PP-Me increases anticancer drug efficiency in breast cancer cells and prevents doxorubicin induced cardiotoxicity.