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dc.creatorSirangelo, I
dc.creatorSapio, L
dc.creatorRagone, A
dc.creatorNaviglio, S
dc.creatorIannuzzi, C
dc.creatorBarone, D
dc.creatorGiordano, A
dc.creatorBorriello, M
dc.date.accessioned2020-12-15T20:17:44Z
dc.date.available2020-12-15T20:17:44Z
dc.date.issued2020-08-01
dc.identifier.issn2072-6643
dc.identifier.issn2072-6643
dc.identifier.doihttp://dx.doi.org/10.34944/dspace/4445
dc.identifier.other32752227 (pubmed)
dc.identifier.urihttp://hdl.handle.net/20.500.12613/4463
dc.description.abstract© 2020 by the authors. Licensee MDPI, Basel, Switzerland. Doxorubicin (doxo) is an effective anticancer compound in several tumor types. However, as a consequence of oxidative stress induction and ROS overproduction, its high cardiotoxicity demands urgent attention. Vanillin possesses antioxidant, antiproliferative, antidepressant and anti-glycating properties. Therefore, we investigated the potential vanillin protective effects against doxo-induced cardiotoxicity in H9c2 cells. Using multiparametric approach, we demonstrated that vanillin restored both cell viability and damage in response to doxo exposure. Contextually, vanillin decreased sub-G1 appearance and caspase-3 and PARP1 activation, reducing the doxo-related apoptosis induction. From a mechanistic point of view, vanillin hindered doxo-induced ROS accumulation and impaired the ERK phosphorylation. Notably, besides the cardioprotective effects, vanillin did not counteract the doxo effectiveness in osteosarcoma cells. Taken together, our results suggest that vanillin ameliorates doxo-induced toxicity in H9c2 cells, opening new avenues for developing alternative therapeutic approaches to prevent the anthracycline-related cardiotoxicity and to improve the long-term outcome of antineoplastic treatment.
dc.format.extent1-17
dc.language.isoen
dc.relation.haspartNutrients
dc.relation.isreferencedbyMDPI AG
dc.rightsCC BY
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.subjectH9c2 cells
dc.subjectROS
dc.subjectantioxidant
dc.subjectcardiotoxicity
dc.subjectchemopreventive agents
dc.subjectdoxorubicin
dc.subjectvanillin
dc.titleVanillin prevents doxorubicin-induced apoptosis and oxidative stress in rat H9c2 cardiomyocytes
dc.typeArticle
dc.type.genreJournal Article
dc.relation.doi10.3390/nu12082317
dc.ada.noteFor Americans with Disabilities Act (ADA) accommodation, including help with reading this content, please contact scholarshare@temple.edu
dc.creator.orcidGiordano, Antonio|0000-0002-5959-016X
dc.date.updated2020-12-15T20:17:40Z
refterms.dateFOA2020-12-15T20:17:45Z


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