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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 s...
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| Published in: | Inflammopharmacology 2022-12, Vol.30 (6), p.2441-2446 |
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| container_end_page | 2446 |
| container_issue | 6 |
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| container_title | Inflammopharmacology |
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| creator | 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 |
| 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. |
| doi_str_mv | 10.1007/s10787-022-01082-z |
| format | article |
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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.</description><identifier>ISSN: 0925-4692</identifier><identifier>EISSN: 1568-5608</identifier><identifier>DOI: 10.1007/s10787-022-01082-z</identifier><identifier>PMID: 36219320</identifier><language>eng</language><publisher>Cham: Springer International Publishing</publisher><subject>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</subject><ispartof>Inflammopharmacology, 2022-12, Vol.30 (6), p.2441-2446</ispartof><rights>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.</rights><rights>2022. The Author(s), under exclusive licence to Springer Nature Switzerland AG.</rights><rights>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.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c446t-31dcd7745fb0fbb25728c46467cde0094dc97f6c74502ecc9bf221104b6845563</citedby><cites>FETCH-LOGICAL-c446t-31dcd7745fb0fbb25728c46467cde0094dc97f6c74502ecc9bf221104b6845563</cites><orcidid>0000-0001-6503-0719</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36219320$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Al-kuraishy, Hayder M.</creatorcontrib><creatorcontrib>Issa, Hajer K.</creatorcontrib><creatorcontrib>Al-Gareeb, Ali I.</creatorcontrib><creatorcontrib>El-Bouseary, Maisra M.</creatorcontrib><creatorcontrib>Youssef, Amal</creatorcontrib><creatorcontrib>Abdelaziz, Ahmed Shaban</creatorcontrib><creatorcontrib>Khalifa, Hesham Ahmed</creatorcontrib><creatorcontrib>Batiha, Gaber El-Saber</creatorcontrib><title>The role of ivabradine in doxorubicin-induced cardiotoxicity: exploring of underlying argument</title><title>Inflammopharmacology</title><addtitle>Inflammopharmacol</addtitle><addtitle>Inflammopharmacology</addtitle><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.</description><subject>Allergology</subject><subject>Animals</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cardiotoxicity - drug therapy</subject><subject>Cardiotoxicity - etiology</subject><subject>Dermatology</subject><subject>Doxorubicin - adverse effects</subject><subject>Gastroenterology</subject><subject>Immunology</subject><subject>Ivabradine - pharmacology</subject><subject>Mice</subject><subject>Original</subject><subject>Original Article</subject><subject>Oxidative Stress</subject><subject>Pharmacology/Toxicology</subject><subject>Rheumatology</subject><subject>Tumor Necrosis Factor-alpha</subject><issn>0925-4692</issn><issn>1568-5608</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><recordid>eNp9kFtLwzAUx4Mobk6_gA_SLxA9SXNpfRBEvMHAl_lqaJN0y-iSka5j26e3dTr0xafDOed_gR9ClwSuCYC8aQjITGKgFAOBjOLdERoSLjLMBWTHaAg55ZiJnA7QWdPMAUBIkZ-iQSooyVMKQ_QxmdkkhtomoUrcuihjYZy3ifOJCZsQ29Jp57HzptXWJLqIxoVV2HTX1fY2sZtlHaLz097eemNjve23Ik7bhfWrc3RSFXVjL77nCL0_PU4eXvD47fn14X6MNWNihVNitJGS8aqEqiwplzTTTDAhtbEAOTM6l5XQnQKo1TovK0oJAVaKjHEu0hG62-cu23Jhje6qY1GrZXSLIm5VKJz6-_FupqZhrXLOKWGkC6D7AB1D00RbHbwEVE9b7Wmrjrb6oq12nenqd-vB8oO3E6R7QbPsIdmo5qGNviPxX-wnhvSOjg</recordid><startdate>20221201</startdate><enddate>20221201</enddate><creator>Al-kuraishy, Hayder M.</creator><creator>Issa, Hajer K.</creator><creator>Al-Gareeb, Ali I.</creator><creator>El-Bouseary, Maisra M.</creator><creator>Youssef, Amal</creator><creator>Abdelaziz, Ahmed Shaban</creator><creator>Khalifa, Hesham Ahmed</creator><creator>Batiha, Gaber El-Saber</creator><general>Springer International Publishing</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-6503-0719</orcidid></search><sort><creationdate>20221201</creationdate><title>The role of ivabradine in doxorubicin-induced cardiotoxicity: exploring of underlying argument</title><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></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c446t-31dcd7745fb0fbb25728c46467cde0094dc97f6c74502ecc9bf221104b6845563</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Allergology</topic><topic>Animals</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cardiotoxicity - drug therapy</topic><topic>Cardiotoxicity - etiology</topic><topic>Dermatology</topic><topic>Doxorubicin - adverse effects</topic><topic>Gastroenterology</topic><topic>Immunology</topic><topic>Ivabradine - pharmacology</topic><topic>Mice</topic><topic>Original</topic><topic>Original Article</topic><topic>Oxidative Stress</topic><topic>Pharmacology/Toxicology</topic><topic>Rheumatology</topic><topic>Tumor Necrosis Factor-alpha</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Al-kuraishy, Hayder M.</creatorcontrib><creatorcontrib>Issa, Hajer K.</creatorcontrib><creatorcontrib>Al-Gareeb, Ali I.</creatorcontrib><creatorcontrib>El-Bouseary, Maisra M.</creatorcontrib><creatorcontrib>Youssef, Amal</creatorcontrib><creatorcontrib>Abdelaziz, Ahmed Shaban</creatorcontrib><creatorcontrib>Khalifa, Hesham Ahmed</creatorcontrib><creatorcontrib>Batiha, Gaber El-Saber</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Inflammopharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Al-kuraishy, Hayder M.</au><au>Issa, Hajer K.</au><au>Al-Gareeb, Ali I.</au><au>El-Bouseary, Maisra M.</au><au>Youssef, Amal</au><au>Abdelaziz, Ahmed Shaban</au><au>Khalifa, Hesham Ahmed</au><au>Batiha, Gaber El-Saber</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The role of ivabradine in doxorubicin-induced cardiotoxicity: exploring of underlying argument</atitle><jtitle>Inflammopharmacology</jtitle><stitle>Inflammopharmacol</stitle><addtitle>Inflammopharmacology</addtitle><date>2022-12-01</date><risdate>2022</risdate><volume>30</volume><issue>6</issue><spage>2441</spage><epage>2446</epage><pages>2441-2446</pages><issn>0925-4692</issn><eissn>1568-5608</eissn><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.</abstract><cop>Cham</cop><pub>Springer International Publishing</pub><pmid>36219320</pmid><doi>10.1007/s10787-022-01082-z</doi><tpages>6</tpages><orcidid>https://orcid.org/0000-0001-6503-0719</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Inflammopharmacology, 2022-12, Vol.30 (6), p.2441-2446 |
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| source | Springer Nature |
| 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 |
| title | The role of ivabradine in doxorubicin-induced cardiotoxicity: exploring of underlying argument |
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