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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 sin...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer International Publishing
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9552141/ https://www.ncbi.nlm.nih.gov/pubmed/36219320 http://dx.doi.org/10.1007/s10787-022-01082-z |
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author | 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 |
author_facet | 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 |
author_sort | Al-kuraishy, Hayder M. |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-9552141 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Springer International Publishing |
record_format | MEDLINE/PubMed |
spelling | pubmed-95521412022-10-11 The role of ivabradine in doxorubicin-induced cardiotoxicity: exploring of underlying argument 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 Inflammopharmacology Original Article 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. Springer International Publishing 2022-10-11 2022 /pmc/articles/PMC9552141/ /pubmed/36219320 http://dx.doi.org/10.1007/s10787-022-01082-z Text en © The Author(s), under exclusive licence to Springer Nature Switzerland AG 2022, Springer Nature or its licensor holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic. |
spellingShingle | Original Article 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 The role of ivabradine in doxorubicin-induced cardiotoxicity: exploring of underlying argument |
title | The role of ivabradine in doxorubicin-induced cardiotoxicity: exploring of underlying argument |
title_full | The role of ivabradine in doxorubicin-induced cardiotoxicity: exploring of underlying argument |
title_fullStr | The role of ivabradine in doxorubicin-induced cardiotoxicity: exploring of underlying argument |
title_full_unstemmed | The role of ivabradine in doxorubicin-induced cardiotoxicity: exploring of underlying argument |
title_short | The role of ivabradine in doxorubicin-induced cardiotoxicity: exploring of underlying argument |
title_sort | role of ivabradine in doxorubicin-induced cardiotoxicity: exploring of underlying argument |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9552141/ https://www.ncbi.nlm.nih.gov/pubmed/36219320 http://dx.doi.org/10.1007/s10787-022-01082-z |
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