The role of ivabradine in doxorubicin-induced cardiotoxicity: exploring of underlying argument.

Abstract

This study investigated the potential role of ivabradine (IVN) in the attenuation of doxorubicin (DXR)-induced cardiotoxicity in rats. A total of 28 Swiss-Albino male mice were used, divided into four equal groups: the negative control did not receive any agents (n = 7), the DXR group received a single dose of DXR 20 mg/kg (n = 7), the treated group A was pretreated with IVN 5 mg/kg plus DXR (n = 7), and the treated group B was pretreated with IVN 10 mg/kg plus DXR (n = 7). The duration of this 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. TNF-α, LDH, MDA, and cTn-I serum levels were higher in the DXR-treated mice compared with the control (P˂0.01). IVN produced a dose-dependent effect in the reduction of MDA and cTn-I compared to DXR-treated mice (P˂0.05). Our findings suggest that IVN is an effective agent in mitigating DXR-induced cardiotoxicity due to its anti-inflammatory and antioxidant effects. IVN illustrated a dose-dependent effect in the attenuation of DXR-induced cardiotoxicity through inhibition of lipid peroxidation and cardiomyocyte injury.