Cardioprotective effects of dapsone against doxorubicin-induced cardiotoxicity in rats
Purpose It has been supposed that cardiac toxicity of doxorubicin is due to its production of free radicals and inflammatory cytokines. Dapsone, an antibiotic drug which is the principal in a multidrug regimen for the treatment of leprosy, is a sulfone with anti-inflammatory and antioxidant immunosu...
Gespeichert in:
| Veröffentlicht in: | Cancer chemotherapy and pharmacology 2020-03, Vol.85 (3), p.563-571 |
|---|---|
| Hauptverfasser: | , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 571 |
|---|---|
| container_issue | 3 |
| container_start_page | 563 |
| container_title | Cancer chemotherapy and pharmacology |
| container_volume | 85 |
| creator | Sheibani, Mohammad Nezamoleslami, Sadaf Faghir-Ghanesefat, Hedyeh Emami, Amir hossein Dehpour, Ahmad Reza |
| description | Purpose
It has been supposed that cardiac toxicity of doxorubicin is due to its production of free radicals and inflammatory cytokines. Dapsone, an antibiotic drug which is the principal in a multidrug regimen for the treatment of leprosy, is a sulfone with anti-inflammatory and antioxidant immunosuppressive properties. Therefore, we designed this study to investigate the possible effects of dapsone on doxorubicin-induced cardiotoxicity.
Methods
Male rats were administrated doxorubicin (2.5 mg/kg) and dapsone (1, 3, 10 mg/kg) intraperitoneally six times in 2 weeks. Then electrocardiographic (ECG) parameters (QRS complexes, RR and QT intervals) alternation, papillary muscle contraction and excitation, and histopathological changes were assessed. Also, the heart tissue levels of malondialdehyde (MDA) as oxidant factor and superoxide dismutase (SOD) as antioxidant enzyme, tumor necrosis factor-alpha (TNF-α) and serum level of CK-MB were analyzed.
Results
Administration of dapsone with doxorubicin significantly reversed alterations induced by doxorubicin in serum levels of CK-MB, ECG parameters, papillary muscle contractility and excitation. Furthermore, the measurement of MDA, SOD and TNF-α tissue level indicated that dapsone significantly reduced oxidative stress and inflammation. These findings were consistent with histopathological analysis.
Conclusion
Dapsone exerts cardioprotective effects on doxorubicin-induced cardiotoxicity through its anti-inflammatory and antioxidant mechanism. |
| doi_str_mv | 10.1007/s00280-019-04019-6 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_journals_2360705420</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2360705420</sourcerecordid><originalsourceid>FETCH-LOGICAL-c441t-1fa2c538290b942fb144090724ce742934ef3c6661ad8b700983d3b3cd71cafb3</originalsourceid><addsrcrecordid>eNp9kElLAzEUx4Motla_gAcZ8Bx9WTrLUYobFLyo15DJUlLspCYZab-9aafqzUsSXv4L74fQJYEbAlDdRgBaAwbSYOC7szxCY8IZxVBzdozGwDjH0wr4CJ3FuAQAThg7RSNGGjJtymqM3mcyaOfXwSejkvsyhbE2v2LhbaHlOvrOFHIhXRdTof3Gh751ynXYdbpXRhdq709-k6dpW7iuCDLFc3Ri5Uc0F4d7gt4e7l9nT3j-8vg8u5tjxTlJmFhJ1ZTVtIG24dS2hHNooKJcmYrThnFjmSrLkkhdtxVAUzPNWqZ0RZS0LZug6yE3L_DZm5jE0vehy5WCshIqmHIKWUUHlQo-xmCsWAe3kmErCIgdSjGgFBmi2KMUZTZdHaL7dmX0r-WHXRawQRDzV7cw4a_7n9hvlfh_Ng</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2360705420</pqid></control><display><type>article</type><title>Cardioprotective effects of dapsone against doxorubicin-induced cardiotoxicity in rats</title><source>MEDLINE</source><source>SpringerLink Journals</source><creator>Sheibani, Mohammad ; Nezamoleslami, Sadaf ; Faghir-Ghanesefat, Hedyeh ; Emami, Amir hossein ; Dehpour, Ahmad Reza</creator><creatorcontrib>Sheibani, Mohammad ; Nezamoleslami, Sadaf ; Faghir-Ghanesefat, Hedyeh ; Emami, Amir hossein ; Dehpour, Ahmad Reza</creatorcontrib><description>Purpose
It has been supposed that cardiac toxicity of doxorubicin is due to its production of free radicals and inflammatory cytokines. Dapsone, an antibiotic drug which is the principal in a multidrug regimen for the treatment of leprosy, is a sulfone with anti-inflammatory and antioxidant immunosuppressive properties. Therefore, we designed this study to investigate the possible effects of dapsone on doxorubicin-induced cardiotoxicity.
Methods
Male rats were administrated doxorubicin (2.5 mg/kg) and dapsone (1, 3, 10 mg/kg) intraperitoneally six times in 2 weeks. Then electrocardiographic (ECG) parameters (QRS complexes, RR and QT intervals) alternation, papillary muscle contraction and excitation, and histopathological changes were assessed. Also, the heart tissue levels of malondialdehyde (MDA) as oxidant factor and superoxide dismutase (SOD) as antioxidant enzyme, tumor necrosis factor-alpha (TNF-α) and serum level of CK-MB were analyzed.
Results
Administration of dapsone with doxorubicin significantly reversed alterations induced by doxorubicin in serum levels of CK-MB, ECG parameters, papillary muscle contractility and excitation. Furthermore, the measurement of MDA, SOD and TNF-α tissue level indicated that dapsone significantly reduced oxidative stress and inflammation. These findings were consistent with histopathological analysis.
Conclusion
Dapsone exerts cardioprotective effects on doxorubicin-induced cardiotoxicity through its anti-inflammatory and antioxidant mechanism.</description><identifier>ISSN: 0344-5704</identifier><identifier>EISSN: 1432-0843</identifier><identifier>DOI: 10.1007/s00280-019-04019-6</identifier><identifier>PMID: 31915967</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Animals ; Anti-Inflammatory Agents - pharmacology ; Antibiotics ; Antioxidants ; Antioxidants - metabolism ; Apoptosis - drug effects ; Cancer Research ; Cardiotoxicity ; Cardiotoxicity - drug therapy ; Cardiotoxicity - metabolism ; Cytokines - metabolism ; Dapsone ; Dapsone - pharmacology ; Diaminodiphenylsulfone ; Doxorubicin ; Doxorubicin - adverse effects ; EKG ; Excitation ; Free radicals ; Heart - drug effects ; Inflammation ; Inflammation - chemically induced ; Inflammation - metabolism ; Leprosy ; Levels ; Male ; Malondialdehyde ; Malondialdehyde - metabolism ; Medicine ; Medicine & Public Health ; Muscle contraction ; Muscles ; Muscular function ; Myocardium - metabolism ; Oncology ; Original Article ; Oxidants ; Oxidative stress ; Oxidative Stress - drug effects ; Oxidizing agents ; Pharmacology/Toxicology ; Protective Agents - pharmacology ; Rats ; Rats, Wistar ; Serum levels ; Superoxide dismutase ; Toxicity ; Tumor Necrosis Factor-alpha - metabolism ; Tumor necrosis factor-TNF ; Tumor necrosis factor-α</subject><ispartof>Cancer chemotherapy and pharmacology, 2020-03, Vol.85 (3), p.563-571</ispartof><rights>Springer-Verlag GmbH Germany, part of Springer Nature 2020</rights><rights>Cancer Chemotherapy and Pharmacology is a copyright of Springer, (2020). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c441t-1fa2c538290b942fb144090724ce742934ef3c6661ad8b700983d3b3cd71cafb3</citedby><cites>FETCH-LOGICAL-c441t-1fa2c538290b942fb144090724ce742934ef3c6661ad8b700983d3b3cd71cafb3</cites><orcidid>0000-0002-8001-5565</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00280-019-04019-6$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00280-019-04019-6$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31915967$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sheibani, Mohammad</creatorcontrib><creatorcontrib>Nezamoleslami, Sadaf</creatorcontrib><creatorcontrib>Faghir-Ghanesefat, Hedyeh</creatorcontrib><creatorcontrib>Emami, Amir hossein</creatorcontrib><creatorcontrib>Dehpour, Ahmad Reza</creatorcontrib><title>Cardioprotective effects of dapsone against doxorubicin-induced cardiotoxicity in rats</title><title>Cancer chemotherapy and pharmacology</title><addtitle>Cancer Chemother Pharmacol</addtitle><addtitle>Cancer Chemother Pharmacol</addtitle><description>Purpose
It has been supposed that cardiac toxicity of doxorubicin is due to its production of free radicals and inflammatory cytokines. Dapsone, an antibiotic drug which is the principal in a multidrug regimen for the treatment of leprosy, is a sulfone with anti-inflammatory and antioxidant immunosuppressive properties. Therefore, we designed this study to investigate the possible effects of dapsone on doxorubicin-induced cardiotoxicity.
Methods
Male rats were administrated doxorubicin (2.5 mg/kg) and dapsone (1, 3, 10 mg/kg) intraperitoneally six times in 2 weeks. Then electrocardiographic (ECG) parameters (QRS complexes, RR and QT intervals) alternation, papillary muscle contraction and excitation, and histopathological changes were assessed. Also, the heart tissue levels of malondialdehyde (MDA) as oxidant factor and superoxide dismutase (SOD) as antioxidant enzyme, tumor necrosis factor-alpha (TNF-α) and serum level of CK-MB were analyzed.
Results
Administration of dapsone with doxorubicin significantly reversed alterations induced by doxorubicin in serum levels of CK-MB, ECG parameters, papillary muscle contractility and excitation. Furthermore, the measurement of MDA, SOD and TNF-α tissue level indicated that dapsone significantly reduced oxidative stress and inflammation. These findings were consistent with histopathological analysis.
Conclusion
Dapsone exerts cardioprotective effects on doxorubicin-induced cardiotoxicity through its anti-inflammatory and antioxidant mechanism.</description><subject>Animals</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>Antibiotics</subject><subject>Antioxidants</subject><subject>Antioxidants - metabolism</subject><subject>Apoptosis - drug effects</subject><subject>Cancer Research</subject><subject>Cardiotoxicity</subject><subject>Cardiotoxicity - drug therapy</subject><subject>Cardiotoxicity - metabolism</subject><subject>Cytokines - metabolism</subject><subject>Dapsone</subject><subject>Dapsone - pharmacology</subject><subject>Diaminodiphenylsulfone</subject><subject>Doxorubicin</subject><subject>Doxorubicin - adverse effects</subject><subject>EKG</subject><subject>Excitation</subject><subject>Free radicals</subject><subject>Heart - drug effects</subject><subject>Inflammation</subject><subject>Inflammation - chemically induced</subject><subject>Inflammation - metabolism</subject><subject>Leprosy</subject><subject>Levels</subject><subject>Male</subject><subject>Malondialdehyde</subject><subject>Malondialdehyde - metabolism</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Muscle contraction</subject><subject>Muscles</subject><subject>Muscular function</subject><subject>Myocardium - metabolism</subject><subject>Oncology</subject><subject>Original Article</subject><subject>Oxidants</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Oxidizing agents</subject><subject>Pharmacology/Toxicology</subject><subject>Protective Agents - pharmacology</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Serum levels</subject><subject>Superoxide dismutase</subject><subject>Toxicity</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumor necrosis factor-α</subject><issn>0344-5704</issn><issn>1432-0843</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kElLAzEUx4Motla_gAcZ8Bx9WTrLUYobFLyo15DJUlLspCYZab-9aafqzUsSXv4L74fQJYEbAlDdRgBaAwbSYOC7szxCY8IZxVBzdozGwDjH0wr4CJ3FuAQAThg7RSNGGjJtymqM3mcyaOfXwSejkvsyhbE2v2LhbaHlOvrOFHIhXRdTof3Gh751ynXYdbpXRhdq709-k6dpW7iuCDLFc3Ri5Uc0F4d7gt4e7l9nT3j-8vg8u5tjxTlJmFhJ1ZTVtIG24dS2hHNooKJcmYrThnFjmSrLkkhdtxVAUzPNWqZ0RZS0LZug6yE3L_DZm5jE0vehy5WCshIqmHIKWUUHlQo-xmCsWAe3kmErCIgdSjGgFBmi2KMUZTZdHaL7dmX0r-WHXRawQRDzV7cw4a_7n9hvlfh_Ng</recordid><startdate>20200301</startdate><enddate>20200301</enddate><creator>Sheibani, Mohammad</creator><creator>Nezamoleslami, Sadaf</creator><creator>Faghir-Ghanesefat, Hedyeh</creator><creator>Emami, Amir hossein</creator><creator>Dehpour, Ahmad Reza</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</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>3V.</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><orcidid>https://orcid.org/0000-0002-8001-5565</orcidid></search><sort><creationdate>20200301</creationdate><title>Cardioprotective effects of dapsone against doxorubicin-induced cardiotoxicity in rats</title><author>Sheibani, Mohammad ; Nezamoleslami, Sadaf ; Faghir-Ghanesefat, Hedyeh ; Emami, Amir hossein ; Dehpour, Ahmad Reza</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c441t-1fa2c538290b942fb144090724ce742934ef3c6661ad8b700983d3b3cd71cafb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Animals</topic><topic>Anti-Inflammatory Agents - pharmacology</topic><topic>Antibiotics</topic><topic>Antioxidants</topic><topic>Antioxidants - metabolism</topic><topic>Apoptosis - drug effects</topic><topic>Cancer Research</topic><topic>Cardiotoxicity</topic><topic>Cardiotoxicity - drug therapy</topic><topic>Cardiotoxicity - metabolism</topic><topic>Cytokines - metabolism</topic><topic>Dapsone</topic><topic>Dapsone - pharmacology</topic><topic>Diaminodiphenylsulfone</topic><topic>Doxorubicin</topic><topic>Doxorubicin - adverse effects</topic><topic>EKG</topic><topic>Excitation</topic><topic>Free radicals</topic><topic>Heart - drug effects</topic><topic>Inflammation</topic><topic>Inflammation - chemically induced</topic><topic>Inflammation - metabolism</topic><topic>Leprosy</topic><topic>Levels</topic><topic>Male</topic><topic>Malondialdehyde</topic><topic>Malondialdehyde - metabolism</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Muscle contraction</topic><topic>Muscles</topic><topic>Muscular function</topic><topic>Myocardium - metabolism</topic><topic>Oncology</topic><topic>Original Article</topic><topic>Oxidants</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>Oxidizing agents</topic><topic>Pharmacology/Toxicology</topic><topic>Protective Agents - pharmacology</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Serum levels</topic><topic>Superoxide dismutase</topic><topic>Toxicity</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><topic>Tumor necrosis factor-TNF</topic><topic>Tumor necrosis factor-α</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sheibani, Mohammad</creatorcontrib><creatorcontrib>Nezamoleslami, Sadaf</creatorcontrib><creatorcontrib>Faghir-Ghanesefat, Hedyeh</creatorcontrib><creatorcontrib>Emami, Amir hossein</creatorcontrib><creatorcontrib>Dehpour, Ahmad Reza</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><jtitle>Cancer chemotherapy and pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sheibani, Mohammad</au><au>Nezamoleslami, Sadaf</au><au>Faghir-Ghanesefat, Hedyeh</au><au>Emami, Amir hossein</au><au>Dehpour, Ahmad Reza</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cardioprotective effects of dapsone against doxorubicin-induced cardiotoxicity in rats</atitle><jtitle>Cancer chemotherapy and pharmacology</jtitle><stitle>Cancer Chemother Pharmacol</stitle><addtitle>Cancer Chemother Pharmacol</addtitle><date>2020-03-01</date><risdate>2020</risdate><volume>85</volume><issue>3</issue><spage>563</spage><epage>571</epage><pages>563-571</pages><issn>0344-5704</issn><eissn>1432-0843</eissn><abstract>Purpose
It has been supposed that cardiac toxicity of doxorubicin is due to its production of free radicals and inflammatory cytokines. Dapsone, an antibiotic drug which is the principal in a multidrug regimen for the treatment of leprosy, is a sulfone with anti-inflammatory and antioxidant immunosuppressive properties. Therefore, we designed this study to investigate the possible effects of dapsone on doxorubicin-induced cardiotoxicity.
Methods
Male rats were administrated doxorubicin (2.5 mg/kg) and dapsone (1, 3, 10 mg/kg) intraperitoneally six times in 2 weeks. Then electrocardiographic (ECG) parameters (QRS complexes, RR and QT intervals) alternation, papillary muscle contraction and excitation, and histopathological changes were assessed. Also, the heart tissue levels of malondialdehyde (MDA) as oxidant factor and superoxide dismutase (SOD) as antioxidant enzyme, tumor necrosis factor-alpha (TNF-α) and serum level of CK-MB were analyzed.
Results
Administration of dapsone with doxorubicin significantly reversed alterations induced by doxorubicin in serum levels of CK-MB, ECG parameters, papillary muscle contractility and excitation. Furthermore, the measurement of MDA, SOD and TNF-α tissue level indicated that dapsone significantly reduced oxidative stress and inflammation. These findings were consistent with histopathological analysis.
Conclusion
Dapsone exerts cardioprotective effects on doxorubicin-induced cardiotoxicity through its anti-inflammatory and antioxidant mechanism.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>31915967</pmid><doi>10.1007/s00280-019-04019-6</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0002-8001-5565</orcidid></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0344-5704 |
| ispartof | Cancer chemotherapy and pharmacology, 2020-03, Vol.85 (3), p.563-571 |
| issn | 0344-5704 1432-0843 |
| language | eng |
| recordid | cdi_proquest_journals_2360705420 |
| source | MEDLINE; SpringerLink Journals |
| subjects | Animals Anti-Inflammatory Agents - pharmacology Antibiotics Antioxidants Antioxidants - metabolism Apoptosis - drug effects Cancer Research Cardiotoxicity Cardiotoxicity - drug therapy Cardiotoxicity - metabolism Cytokines - metabolism Dapsone Dapsone - pharmacology Diaminodiphenylsulfone Doxorubicin Doxorubicin - adverse effects EKG Excitation Free radicals Heart - drug effects Inflammation Inflammation - chemically induced Inflammation - metabolism Leprosy Levels Male Malondialdehyde Malondialdehyde - metabolism Medicine Medicine & Public Health Muscle contraction Muscles Muscular function Myocardium - metabolism Oncology Original Article Oxidants Oxidative stress Oxidative Stress - drug effects Oxidizing agents Pharmacology/Toxicology Protective Agents - pharmacology Rats Rats, Wistar Serum levels Superoxide dismutase Toxicity Tumor Necrosis Factor-alpha - metabolism Tumor necrosis factor-TNF Tumor necrosis factor-α |
| title | Cardioprotective effects of dapsone against doxorubicin-induced cardiotoxicity in rats |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-02T09%3A31%3A01IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Cardioprotective%20effects%20of%20dapsone%20against%20doxorubicin-induced%20cardiotoxicity%20in%20rats&rft.jtitle=Cancer%20chemotherapy%20and%20pharmacology&rft.au=Sheibani,%20Mohammad&rft.date=2020-03-01&rft.volume=85&rft.issue=3&rft.spage=563&rft.epage=571&rft.pages=563-571&rft.issn=0344-5704&rft.eissn=1432-0843&rft_id=info:doi/10.1007/s00280-019-04019-6&rft_dat=%3Cproquest_cross%3E2360705420%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2360705420&rft_id=info:pmid/31915967&rfr_iscdi=true |