Nebivolol and atenolol roles in doxorubicin-induced cardiotoxicity

Background: This study investigated the potential role of ivabradine (Nebivolol and Atenolol) in the attenuation of doxorubicin induced cardiotoxicity in mice. So we will seek the role of nebivolol and atenolol in reducing cardiotoxicity induced by doxorubicin in this experimental study. Aims: To investigate the potential roles of nebivolol and atenolol in the attenuation of doxorubicin (DXR)-induced cardiotoxicity in mice. Materials and Methods: A total of 42 Swiss-Albino male and female mice were used, which were divided into six equal groups: A negative control, a group 1 not received any agents, group 2 (DXR group) received a single dose of DXR 15 mg/kg, treated group 3 was pretreated with nebivolol 15 mg/kg plus DXR. Treated group 4 was pretreated with nebivolol 30 mg/kg plus DXR. Treated group 5 was pretreated with Atenolol 45 mg/kg plus DXR, and treated group 6 was pretreated with atenolol 90 mg/kg plus DXR. The duration of the study was 10 days. Inflammatory biomarkers including tumor necrosis factor-alpha (TNF-α), lactate dehydrogenase (LDH), malondialdehyde (MDA), and cardiac troponin (cTn-I) serum levels were measured. SPSS version 28.00 was used for data analysis. Results: TNF-α, LDH, MDA, and cTn-I serum levels were higher in the DXR-treated mice as compared to the control (P < 0.05). Nebivolol and atenolol produced a dose-dependent effect in the reduction of TNF-α, LDH, MDA, and cTn-I serum levels as compared to the DXR-treated mice (P < 0.05). Conclusion: Atenolol and nebivolol were effective agents in the mitigation of DXR-induced cardiotoxicity by their anti-inflammatory effects of both atenolol and nebivolol and antioxidant effects of nebivolol. Atenolol and nebivolol illustrated a dose-dependent effect in the attenuation of DXR-induced cardiotoxicity through inhibition of lipid peroxidation and cardiomyocyte injury.