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

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 s...

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Published in:Inflammopharmacology 2022-12, Vol.30 (6), p.2441-2446
Main Authors: Al-kuraishy, Hayder M., Issa, Hajer K., Al-Gareeb, Ali I., El-Bouseary, Maisra M., Youssef, Amal, Abdelaziz, Ahmed Shaban, Khalifa, Hesham Ahmed, Batiha, Gaber El-Saber
Format: Article
Language:English
Subjects:
Allergology
Animals
Biomedical and Life Sciences
Biomedicine
Cardiotoxicity - drug therapy
Cardiotoxicity - etiology
Dermatology
Doxorubicin - adverse effects
Gastroenterology
Immunology
Ivabradine - pharmacology
Mice
Original
Original Article
Oxidative Stress
Pharmacology/Toxicology
Rheumatology
Tumor Necrosis Factor-alpha
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Summary: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.
ISSN:0925-4692
1568-5608
DOI:10.1007/s10787-022-01082-z