Aspernolide F, as a new cardioprotective butyrolactone against doxorubicin-induced cardiotoxicity
Endophytic fungi have known as a promising source of secondary metabolites. γ-Butyrolactones are a class of metabolites reported from Aspergillus genus, which attracted much attention for their bioactivities. This study aimed to assess the potential cardioprotective effects of aspernolide F (AF) sep...
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| Veröffentlicht in: | International immunopharmacology 2019-07, Vol.72, p.429-436 |
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| creator | El-Agamy, Dina S. Ibrahim, Sabrin R.M. Ahmed, Nishat Khoshhal, Saad Abo-Haded, Hany M. Elkablawy, Mohamed A. Aljuhani, Naif Mohamed, Gamal A. |
| description | Endophytic fungi have known as a promising source of secondary metabolites. γ-Butyrolactones are a class of metabolites reported from Aspergillus genus, which attracted much attention for their bioactivities. This study aimed to assess the potential cardioprotective effects of aspernolide F (AF) separated from the endophytic fungus A. terreus against doxorubicin (DOX)-induced cardiotoxic effects in rats. Animals were treated with two different doses of AF for 10 days prior to DOX injection. Electrocardiographic (ECG), biochemical, histopathological and immunohistochemical analyses were performed. Results have shown that AF effectively protected against DOX-induced cardiac damage as AF counteracted DOX-induced ECG abnormalities and attenuated serum markers of cardiotoxicity (creatine kinase-MB, lactate dehydrogenase, troponin I, and troponin T). Histopathological examination of cardiac tissue revealed a remarkable improvement in DOX-induced lesions. In addition, AF ameliorated DOX-induced oxidative damage and increased the levels of antioxidants in cardiac tissues. AF treatment inhibited the activation of nuclear factor-κB (NF-κB) and decreased the immuno-expression of NF-κB in cardiac tissue. Furthermore, AF caused a marked lowering in the level of inflammatory cytokines (nitric oxide, tumor necrosis factor-α, and interleukin-6) in the cardiac tissue. Collectively, this study demonstrates the cardioprotective activity of AF against DOX-induced cardiac damage which may be due to its antioxidant and anti-inflammatory activities.
•Aspernolide F (AF) was separated from the endophytic fungus Aspergillus terreus.•AF possessed a cardioprotective effect against doxorubicin (DOX)-induced cardiotoxic effects.•AF attenuated DOX-induced oxidative damage and enhanced antioxidants.•AF suppressed inflammatory response via inhibition of the activation of nuclear factor-κB (NF-κB). |
| doi_str_mv | 10.1016/j.intimp.2019.04.045 |
| format | Article |
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•Aspernolide F (AF) was separated from the endophytic fungus Aspergillus terreus.•AF possessed a cardioprotective effect against doxorubicin (DOX)-induced cardiotoxic effects.•AF attenuated DOX-induced oxidative damage and enhanced antioxidants.•AF suppressed inflammatory response via inhibition of the activation of nuclear factor-κB (NF-κB).</description><identifier>ISSN: 1567-5769</identifier><identifier>EISSN: 1878-1705</identifier><identifier>DOI: 10.1016/j.intimp.2019.04.045</identifier><identifier>PMID: 31030099</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Abnormalities ; Animals ; Antibiotics, Antineoplastic ; Antioxidants ; Antioxidants - isolation & purification ; Antioxidants - pharmacology ; Antioxidants - therapeutic use ; Aspergillus ; Aspergillus terreus ; Aspernolide F ; Butyrolactone ; Calcium-binding protein ; Cardiotonic Agents - isolation & purification ; Cardiotonic Agents - pharmacology ; Cardiotonic Agents - therapeutic use ; Cardiotoxicity ; Cardiotoxicity - drug therapy ; Cardiotoxicity - metabolism ; Creatine ; Creatine kinase ; Cytokines ; Doxorubicin ; EKG ; Endophytes ; Fungi ; Heart ; Inflammation ; Interleukin 6 ; Interleukin-6 - metabolism ; Kinases ; L-Lactate dehydrogenase ; Lactate dehydrogenase ; Lactic acid ; Lesions ; Male ; Metabolites ; Myocardium - metabolism ; Myocardium - pathology ; NF-kappa B - metabolism ; NF-κB ; NF-κB protein ; Nitric oxide ; Nitric Oxide - metabolism ; Oxidative Stress - drug effects ; Rats, Wistar ; Secondary metabolites ; Tissues ; Troponin ; Troponin I ; Troponin T ; Tumor Necrosis Factor-alpha - metabolism ; Tumor necrosis factor-α ; γ-Butyrolactones</subject><ispartof>International immunopharmacology, 2019-07, Vol.72, p.429-436</ispartof><rights>2019 Elsevier B.V.</rights><rights>Copyright © 2019 Elsevier B.V. All rights reserved.</rights><rights>Copyright Elsevier BV Jul 2019</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c390t-608e1833a1cb8431e681728ec0aac5b4c1121daeacce4e1e7b7d3590657bee823</citedby><cites>FETCH-LOGICAL-c390t-608e1833a1cb8431e681728ec0aac5b4c1121daeacce4e1e7b7d3590657bee823</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.intimp.2019.04.045$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>315,782,786,3552,27931,27932,46002</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31030099$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>El-Agamy, Dina S.</creatorcontrib><creatorcontrib>Ibrahim, Sabrin R.M.</creatorcontrib><creatorcontrib>Ahmed, Nishat</creatorcontrib><creatorcontrib>Khoshhal, Saad</creatorcontrib><creatorcontrib>Abo-Haded, Hany M.</creatorcontrib><creatorcontrib>Elkablawy, Mohamed A.</creatorcontrib><creatorcontrib>Aljuhani, Naif</creatorcontrib><creatorcontrib>Mohamed, Gamal A.</creatorcontrib><title>Aspernolide F, as a new cardioprotective butyrolactone against doxorubicin-induced cardiotoxicity</title><title>International immunopharmacology</title><addtitle>Int Immunopharmacol</addtitle><description>Endophytic fungi have known as a promising source of secondary metabolites. γ-Butyrolactones are a class of metabolites reported from Aspergillus genus, which attracted much attention for their bioactivities. This study aimed to assess the potential cardioprotective effects of aspernolide F (AF) separated from the endophytic fungus A. terreus against doxorubicin (DOX)-induced cardiotoxic effects in rats. Animals were treated with two different doses of AF for 10 days prior to DOX injection. Electrocardiographic (ECG), biochemical, histopathological and immunohistochemical analyses were performed. Results have shown that AF effectively protected against DOX-induced cardiac damage as AF counteracted DOX-induced ECG abnormalities and attenuated serum markers of cardiotoxicity (creatine kinase-MB, lactate dehydrogenase, troponin I, and troponin T). Histopathological examination of cardiac tissue revealed a remarkable improvement in DOX-induced lesions. In addition, AF ameliorated DOX-induced oxidative damage and increased the levels of antioxidants in cardiac tissues. AF treatment inhibited the activation of nuclear factor-κB (NF-κB) and decreased the immuno-expression of NF-κB in cardiac tissue. Furthermore, AF caused a marked lowering in the level of inflammatory cytokines (nitric oxide, tumor necrosis factor-α, and interleukin-6) in the cardiac tissue. Collectively, this study demonstrates the cardioprotective activity of AF against DOX-induced cardiac damage which may be due to its antioxidant and anti-inflammatory activities.
•Aspernolide F (AF) was separated from the endophytic fungus Aspergillus terreus.•AF possessed a cardioprotective effect against doxorubicin (DOX)-induced cardiotoxic effects.•AF attenuated DOX-induced oxidative damage and enhanced antioxidants.•AF suppressed inflammatory response via inhibition of the activation of nuclear factor-κB (NF-κB).</description><subject>Abnormalities</subject><subject>Animals</subject><subject>Antibiotics, Antineoplastic</subject><subject>Antioxidants</subject><subject>Antioxidants - isolation & purification</subject><subject>Antioxidants - pharmacology</subject><subject>Antioxidants - therapeutic use</subject><subject>Aspergillus</subject><subject>Aspergillus terreus</subject><subject>Aspernolide F</subject><subject>Butyrolactone</subject><subject>Calcium-binding protein</subject><subject>Cardiotonic Agents - isolation & purification</subject><subject>Cardiotonic Agents - pharmacology</subject><subject>Cardiotonic Agents - therapeutic use</subject><subject>Cardiotoxicity</subject><subject>Cardiotoxicity - drug therapy</subject><subject>Cardiotoxicity - metabolism</subject><subject>Creatine</subject><subject>Creatine kinase</subject><subject>Cytokines</subject><subject>Doxorubicin</subject><subject>EKG</subject><subject>Endophytes</subject><subject>Fungi</subject><subject>Heart</subject><subject>Inflammation</subject><subject>Interleukin 6</subject><subject>Interleukin-6 - metabolism</subject><subject>Kinases</subject><subject>L-Lactate dehydrogenase</subject><subject>Lactate dehydrogenase</subject><subject>Lactic acid</subject><subject>Lesions</subject><subject>Male</subject><subject>Metabolites</subject><subject>Myocardium - metabolism</subject><subject>Myocardium - pathology</subject><subject>NF-kappa B - metabolism</subject><subject>NF-κB</subject><subject>NF-κB protein</subject><subject>Nitric oxide</subject><subject>Nitric Oxide - metabolism</subject><subject>Oxidative Stress - drug effects</subject><subject>Rats, Wistar</subject><subject>Secondary metabolites</subject><subject>Tissues</subject><subject>Troponin</subject><subject>Troponin I</subject><subject>Troponin T</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Tumor necrosis factor-α</subject><subject>γ-Butyrolactones</subject><issn>1567-5769</issn><issn>1878-1705</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kNtKAzEQhoMont9AZMFbt87sKdkbQcQTCN7odcgmo6S0SU2y2r69Ka1eCgMzDP8_h4-xM4QJAnZX04l1yc4Xkwqwn0CTo91hhyi4KJFDu5vrtuNly7v-gB3FOAXI_Qb32UGNUAP0_SFTN3FBwfmZNVTcXxYqFqpw9F1oFYz1i-AT6WS_qBjGtAp-pnTyjgr1oayLqTB-6cM4WG1daZ0ZNZmtNfll7qbVCdt7V7NIp9t8zN7u715vH8vnl4en25vnUtc9pLIDQSjqWqEeRFMjdQJ5JUiDUrodGo1YoVGktKaGkPjATd320LV8IBJVfcwuNnPzzZ8jxSSnfgwur5RV1VRcgOCYVc1GpYOPMdC7XAQ7V2ElEeSaq5zKDVe55iqhydFm2_l2-DjMyfyZfkFmwfVGQPnFL0tBRm3JZRw2ZIDSePv_hh-BII0Z</recordid><startdate>201907</startdate><enddate>201907</enddate><creator>El-Agamy, Dina S.</creator><creator>Ibrahim, Sabrin R.M.</creator><creator>Ahmed, Nishat</creator><creator>Khoshhal, Saad</creator><creator>Abo-Haded, Hany M.</creator><creator>Elkablawy, Mohamed A.</creator><creator>Aljuhani, Naif</creator><creator>Mohamed, Gamal A.</creator><general>Elsevier B.V</general><general>Elsevier BV</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>7QO</scope><scope>7T5</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope></search><sort><creationdate>201907</creationdate><title>Aspernolide F, as a new cardioprotective butyrolactone against doxorubicin-induced cardiotoxicity</title><author>El-Agamy, Dina S. ; Ibrahim, Sabrin R.M. ; Ahmed, Nishat ; Khoshhal, Saad ; Abo-Haded, Hany M. ; Elkablawy, Mohamed A. ; Aljuhani, Naif ; Mohamed, Gamal A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c390t-608e1833a1cb8431e681728ec0aac5b4c1121daeacce4e1e7b7d3590657bee823</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Abnormalities</topic><topic>Animals</topic><topic>Antibiotics, Antineoplastic</topic><topic>Antioxidants</topic><topic>Antioxidants - isolation & purification</topic><topic>Antioxidants - pharmacology</topic><topic>Antioxidants - therapeutic use</topic><topic>Aspergillus</topic><topic>Aspergillus terreus</topic><topic>Aspernolide F</topic><topic>Butyrolactone</topic><topic>Calcium-binding protein</topic><topic>Cardiotonic Agents - isolation & purification</topic><topic>Cardiotonic Agents - pharmacology</topic><topic>Cardiotonic Agents - therapeutic use</topic><topic>Cardiotoxicity</topic><topic>Cardiotoxicity - drug therapy</topic><topic>Cardiotoxicity - metabolism</topic><topic>Creatine</topic><topic>Creatine kinase</topic><topic>Cytokines</topic><topic>Doxorubicin</topic><topic>EKG</topic><topic>Endophytes</topic><topic>Fungi</topic><topic>Heart</topic><topic>Inflammation</topic><topic>Interleukin 6</topic><topic>Interleukin-6 - metabolism</topic><topic>Kinases</topic><topic>L-Lactate dehydrogenase</topic><topic>Lactate dehydrogenase</topic><topic>Lactic acid</topic><topic>Lesions</topic><topic>Male</topic><topic>Metabolites</topic><topic>Myocardium - metabolism</topic><topic>Myocardium - pathology</topic><topic>NF-kappa B - metabolism</topic><topic>NF-κB</topic><topic>NF-κB protein</topic><topic>Nitric oxide</topic><topic>Nitric Oxide - metabolism</topic><topic>Oxidative Stress - drug effects</topic><topic>Rats, Wistar</topic><topic>Secondary metabolites</topic><topic>Tissues</topic><topic>Troponin</topic><topic>Troponin I</topic><topic>Troponin T</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><topic>Tumor necrosis factor-α</topic><topic>γ-Butyrolactones</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>El-Agamy, Dina S.</creatorcontrib><creatorcontrib>Ibrahim, Sabrin R.M.</creatorcontrib><creatorcontrib>Ahmed, Nishat</creatorcontrib><creatorcontrib>Khoshhal, Saad</creatorcontrib><creatorcontrib>Abo-Haded, Hany M.</creatorcontrib><creatorcontrib>Elkablawy, Mohamed A.</creatorcontrib><creatorcontrib>Aljuhani, Naif</creatorcontrib><creatorcontrib>Mohamed, Gamal A.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Immunology Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><jtitle>International immunopharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>El-Agamy, Dina S.</au><au>Ibrahim, Sabrin R.M.</au><au>Ahmed, Nishat</au><au>Khoshhal, Saad</au><au>Abo-Haded, Hany M.</au><au>Elkablawy, Mohamed A.</au><au>Aljuhani, Naif</au><au>Mohamed, Gamal A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Aspernolide F, as a new cardioprotective butyrolactone against doxorubicin-induced cardiotoxicity</atitle><jtitle>International immunopharmacology</jtitle><addtitle>Int Immunopharmacol</addtitle><date>2019-07</date><risdate>2019</risdate><volume>72</volume><spage>429</spage><epage>436</epage><pages>429-436</pages><issn>1567-5769</issn><eissn>1878-1705</eissn><abstract>Endophytic fungi have known as a promising source of secondary metabolites. γ-Butyrolactones are a class of metabolites reported from Aspergillus genus, which attracted much attention for their bioactivities. This study aimed to assess the potential cardioprotective effects of aspernolide F (AF) separated from the endophytic fungus A. terreus against doxorubicin (DOX)-induced cardiotoxic effects in rats. Animals were treated with two different doses of AF for 10 days prior to DOX injection. Electrocardiographic (ECG), biochemical, histopathological and immunohistochemical analyses were performed. Results have shown that AF effectively protected against DOX-induced cardiac damage as AF counteracted DOX-induced ECG abnormalities and attenuated serum markers of cardiotoxicity (creatine kinase-MB, lactate dehydrogenase, troponin I, and troponin T). Histopathological examination of cardiac tissue revealed a remarkable improvement in DOX-induced lesions. In addition, AF ameliorated DOX-induced oxidative damage and increased the levels of antioxidants in cardiac tissues. AF treatment inhibited the activation of nuclear factor-κB (NF-κB) and decreased the immuno-expression of NF-κB in cardiac tissue. Furthermore, AF caused a marked lowering in the level of inflammatory cytokines (nitric oxide, tumor necrosis factor-α, and interleukin-6) in the cardiac tissue. Collectively, this study demonstrates the cardioprotective activity of AF against DOX-induced cardiac damage which may be due to its antioxidant and anti-inflammatory activities.
•Aspernolide F (AF) was separated from the endophytic fungus Aspergillus terreus.•AF possessed a cardioprotective effect against doxorubicin (DOX)-induced cardiotoxic effects.•AF attenuated DOX-induced oxidative damage and enhanced antioxidants.•AF suppressed inflammatory response via inhibition of the activation of nuclear factor-κB (NF-κB).</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>31030099</pmid><doi>10.1016/j.intimp.2019.04.045</doi><tpages>8</tpages></addata></record> |
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| subjects | Abnormalities Animals Antibiotics, Antineoplastic Antioxidants Antioxidants - isolation & purification Antioxidants - pharmacology Antioxidants - therapeutic use Aspergillus Aspergillus terreus Aspernolide F Butyrolactone Calcium-binding protein Cardiotonic Agents - isolation & purification Cardiotonic Agents - pharmacology Cardiotonic Agents - therapeutic use Cardiotoxicity Cardiotoxicity - drug therapy Cardiotoxicity - metabolism Creatine Creatine kinase Cytokines Doxorubicin EKG Endophytes Fungi Heart Inflammation Interleukin 6 Interleukin-6 - metabolism Kinases L-Lactate dehydrogenase Lactate dehydrogenase Lactic acid Lesions Male Metabolites Myocardium - metabolism Myocardium - pathology NF-kappa B - metabolism NF-κB NF-κB protein Nitric oxide Nitric Oxide - metabolism Oxidative Stress - drug effects Rats, Wistar Secondary metabolites Tissues Troponin Troponin I Troponin T Tumor Necrosis Factor-alpha - metabolism Tumor necrosis factor-α γ-Butyrolactones |
| title | Aspernolide F, as a new cardioprotective butyrolactone against doxorubicin-induced cardiotoxicity |
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