Effect of Cucumis melo var. agrestis Naudin on doxorubicin-induced cardiotoxicity in rats

Abstract

Purpose: Doxorubicin (DOX), a chemotherapeutic antibiotic, induces toxicity by also targeting non-cancerous cells. Cucumis melo var. agrestis Naudin (CM), a plant belonging to the Cucurbitaceae family with high antioxidant content, is examined in this study for its potential impact on DOX-induced cardiac damage at different doses. Materials and Methods: 30 male rats were randomly divided into 5 groups, with 6 animals in each group: Control group, which received distilled water by gavage for 10 days, and intraperitoneal (i.p.) normal saline application on the 5th day of the experiment. The DOX group consisted of rats receiving a single i.p. dose of 15 mg/kg DOX on the 5th day of the experiment. Rats receiving a single intraperitoneal dose of 15 mg/kg DOX on the 5th day of the experiment were subjected to gavage for 10 days with doses of 100 mg/kg (DOX+CM100), 250 mg/kg (DOX+CM250), and 500 mg/kg (DOX+CM500) of CM, respectively. 24 hours after the last drug administration, the experimental animals were sacrificed under anesthesia. Heart tissue was examined histochemically and immunohistochemically. Results: At the end of the experiment, histopathological examination of the heart tissue; Compared to the control group, histolopathological findings such as degeneration of muscle fibers, vacuole-like structures between muscle fibers, congestion in vessels, and edema between collaterals were observed in the DOX group. These findings significantly decreased in the DOX+CM250 treatment group. While an increase in Caspase-3, HSP 70 and NF-κB-p65 immunoreactivities was observed in the DOX group (+++); In the DOX+CM250 group, these findings decreased significantly (+). Conclusion: DOX accelerated the apoptotic process, increased intracellular and oxidative stress, and triggered an inflammatory response, as demonstrated histochemically and immunohistochemically. CM administered at a dose of 250 mg/kg expedited cardiac remodeling.