Eicosapentaenoic acid and vitamin e against doxorubicin-induced cardiac and renal damages: Role of cytochrome c and inos
dc.Affiliation | October University for modern sciences and Arts (MSA) | |
dc.contributor.author | Fayez A.M. | |
dc.contributor.author | Zaafan M.A. | |
dc.contributor.other | Pharmacology and Toxicology Department | |
dc.contributor.other | Faculty of Pharmacy | |
dc.contributor.other | October University for Modern Sciences | |
dc.contributor.other | Arts | |
dc.contributor.other | Egypt | |
dc.date.accessioned | 2020-01-09T20:40:50Z | |
dc.date.available | 2020-01-09T20:40:50Z | |
dc.date.issued | 2018 | |
dc.description | Scopus | |
dc.description.abstract | Background: The current study aimed to evaluate the mechanisms involved in protection against doxorubicin-induced cardiac and renal toxicities upon treatment with eicosapentaenoic acid and vitamin E. Methods: Rats were randomly assigned to 4 groups: normal control, doxorubicin inducted control, eicosapentaenoic acid treated group and a final group pretreated with vitamin E. Lipid peroxidation, reduced glutathione (GSH) and tumor necrosis factor-alpha (TNF-?) contents as well as glutathione peroxidase (GPx), superoxide dismutase (SOD) and myeloperoxidase (MPO) activities were assessed. Moreover, hearts were used for immunohistochemical detection of the pro-apoptotic protein cytochrome c expression, while the kidneys were used for detection of inducible nitric oxide synthase (iNOS) expression. Results: Eicosapentaenoic acid and vitamin E produced significant protection from doxorubicin-induced cardiac and renal toxicities. The suggested mechanisms for protection included decreased cytochrome c and iNOS expression as well as markedly decreased lipid peroxides and TNF-? contents accompanied with increased GSH content as compared to the doxorubicin control group. Moreover, there was marked increase in GPx and SOD activities accompanied by significant suppression of MPO activity. Conclusion: The present study demonstrated the potent protective effects of eicosapentaenoic acid and vitamin E from doxorubicin induced cardiac and renal toxicities through their potent anti-oxidant, anti-inflammatory and anti-apoptotic properties. Hence, eicosapentaenoic acid and vitamin E could be promising protective agents against doxorubicintoxicity. � 2019, Academy of Medical Sciences of I.R. Iran. All rights reserved. | en_US |
dc.description.uri | https://www.scimagojr.com/journalsearch.php?q=27539&tip=sid&clean=0 | |
dc.identifier.doi | https://doi.org/ | |
dc.identifier.issn | 10292977 | |
dc.identifier.other | https://doi.org/ | |
dc.identifier.uri | https://t.ly/pyGM9 | |
dc.language.iso | English | en_US |
dc.publisher | Academy of Medical Sciences of I.R. Iran | en_US |
dc.relation.ispartofseries | Archives of Iranian Medicine | |
dc.relation.ispartofseries | 21 | |
dc.subject | Anti-inflammatory | en_US |
dc.subject | Cytochrome c | en_US |
dc.subject | Doxorubicin | en_US |
dc.subject | Eicosapentaenoic acid | en_US |
dc.subject | INOS | en_US |
dc.subject | Vitamin E Cite this article as: Fayez AM | en_US |
dc.subject | Zaafan MA. Eicosapentaenoic acid and vitamin E against doxorubicin-induced cardiac and renal | en_US |
dc.subject | alpha tocopherol | en_US |
dc.subject | creatine kinase MB | en_US |
dc.subject | cytochrome c | en_US |
dc.subject | doxorubicin | en_US |
dc.subject | glutathione | en_US |
dc.subject | glutathione peroxidase | en_US |
dc.subject | icosapentaenoic acid | en_US |
dc.subject | inducible nitric oxide synthase | en_US |
dc.subject | lipid peroxide | en_US |
dc.subject | malonaldehyde | en_US |
dc.subject | myeloperoxidase | en_US |
dc.subject | superoxide dismutase | en_US |
dc.subject | tumor necrosis factor | en_US |
dc.subject | alpha tocopherol | en_US |
dc.subject | antineoplastic antibiotic | en_US |
dc.subject | cytochrome c | en_US |
dc.subject | doxorubicin | en_US |
dc.subject | glutathione peroxidase | en_US |
dc.subject | icosapentaenoic acid | en_US |
dc.subject | inducible nitric oxide synthase | en_US |
dc.subject | Nos2 protein, rat | en_US |
dc.subject | superoxide dismutase | en_US |
dc.subject | animal experiment | en_US |
dc.subject | animal model | en_US |
dc.subject | animal tissue | en_US |
dc.subject | antiapoptotic activity | en_US |
dc.subject | antiinflammatory activity | en_US |
dc.subject | antioxidant activity | en_US |
dc.subject | apoptosis | en_US |
dc.subject | Article | en_US |
dc.subject | bleeding | en_US |
dc.subject | cell infiltration | en_US |
dc.subject | controlled study | en_US |
dc.subject | enzyme activity | en_US |
dc.subject | enzyme linked immunosorbent assay | en_US |
dc.subject | heart injury | en_US |
dc.subject | immunohistochemistry | en_US |
dc.subject | inflammation | en_US |
dc.subject | kidney injury | en_US |
dc.subject | lipid peroxidation | en_US |
dc.subject | male | en_US |
dc.subject | nonhuman | en_US |
dc.subject | protein expression | en_US |
dc.subject | rat | en_US |
dc.subject | swelling | en_US |
dc.subject | tissue degeneration | en_US |
dc.subject | animal | en_US |
dc.subject | cardiac muscle | en_US |
dc.subject | drug effect | en_US |
dc.subject | heart | en_US |
dc.subject | kidney | en_US |
dc.subject | metabolism | en_US |
dc.subject | pathology | en_US |
dc.subject | Wistar rat | en_US |
dc.subject | Animals | en_US |
dc.subject | Antibiotics, Antineoplastic | en_US |
dc.subject | Cytochromes c | en_US |
dc.subject | Doxorubicin | en_US |
dc.subject | Eicosapentaenoic Acid | en_US |
dc.subject | Glutathione Peroxidase | en_US |
dc.subject | Heart | en_US |
dc.subject | Kidney | en_US |
dc.subject | Lipid Peroxidation | en_US |
dc.subject | Male | en_US |
dc.subject | Myocardium | en_US |
dc.subject | Nitric Oxide Synthase Type II | en_US |
dc.subject | Rats | en_US |
dc.subject | Rats, Wistar | en_US |
dc.subject | Superoxide Dismutase | en_US |
dc.subject | Vitamin E | en_US |
dc.title | Eicosapentaenoic acid and vitamin e against doxorubicin-induced cardiac and renal damages: Role of cytochrome c and inos | en_US |
dc.type | Article | en_US |
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dcterms.source | Scopus |