Background: Doxorubicin (DOX) is an anticancer drug with significant clinical implications; however its utilization is limited due to its significant adverse effects especially on the cardiac muscle.
Objectives: The current study aimed to examine improving the cardio-protective activity of Captopril (CAP) against Doxorubicin (DOX) induced cardiotoxicity via co-administration with allicin and investigate the potential underlying mechanisms.
Materials and methods: 40 Sprague dewily rats were allocated into five groups, consisting of a Control group, DOX group, DOX + CAP group, DOX + allicin group and DOX + CAP + allicin group. Biochemical and histological evaluations of the myocardial tissue were conducted. The study utilized myocardium specimens to determine the levels of lipid peroxide product (MDA) and superoxide dismutase (SOD) in addition to  reduced glutathione (GSH), while the inflammatory mediators IL-1β and TNF-α in addition to cardiac troponin I and creatine kinase were determined in rats' sera.
Results: either CAP or allicin administration resulted in a significant reduction in the biochemical indicators of cardiotoxicity. Both CAP and allicin ameliorate Dox impact on inflammation and oxidative stress markers, whereas allicin showed higher impact than CAP. However, the combined administration of CAP with allicin produced much more ameliorative effects. Histopathological, the concurrent administration of both medications produced higher effect to mitigate DOX-induced myocardial damage than use any of them solely.
Conclusion: this study revealed that the cardioprotective activities of CAP can be greatly enhanced by co-administration with allicin via dramatically reduction in both oxidative stress and inflammatory status that contribute to DOX induced cardiotoxicity.