Protective effects of necrostatin-1 on doxorubicin-induced cardiotoxicity in rat heart

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dc.authorid0000-0001-6607-836Xen_US
dc.authorid0000-0001-5591-7607en_US
dc.authorid0000-0003-3232-7019en_US
dc.authorid0000-0003-4661-9784en_US
dc.authorid0000-0002-9988-9385en_US
dc.contributor.authorÖzgen, Zeynep Erdoğmuş
dc.contributor.authorErdinç, Meral
dc.contributor.authorKelle, İlker
dc.contributor.authorErdinç, Levent
dc.contributor.authorNergiz, Yusuf
dc.date.accessioned2023-03-15T06:50:57Z
dc.date.available2023-03-15T06:50:57Z
dc.date.issued2022en_US
dc.departmentDicle Üniversitesi, Eczacılık Fakültesi, Eczacılık Meslek Bililmleri Bölümüen_US
dc.description.abstractBackground: Doxorubicin (Dox) is one of the most effective antineoplastic drugs which has severe cardiotoxic effects, limiting its clinical usage. Though the exact mechanism of doxorubicin-induced cardiotoxicity is yet to be elucidated, it is shown that production of reactive oxygen species (ROS) increases oxidative stress and leads to cardiomyocyte apoptosis and necroptosis which is also defined as a programmed cell death. Purpose: In the present study, we investigate the effects of necrostatin-1 (Nec-1)-an inhibitor of receptor interaction proteins 1 (RIP1) and necroptosis-on doxorubicin-induced cardiotoxicity in rats. Research Design: Hearts were isolated and perfused by the Langendorff system in all four groups. Perfusion pressure (PP), left ventricular developed pressure (LVDP) and heart rate per minute (HR), LV (dP/dt) max, and LV (dP/dt) min which shows cardiac contractility and relaxation were recorded. Results: Results showed that PP significantly increased with Dox treatment and significantly decreased with Nec-1 treatment, while HR, LVDP, LV (dP/dt) max, and LV (dP/dt) min values significantly decreased with the Dox-treated group and significantly increased with Nec-1 treatment. Also with Nec-1 treatment, gene expression levels of anti-apoptotic Bcl-2 significantly increased and pro-apoptotic protein Bax, apoptotic marker caspase-3, and Nox-2 significantly decreased compared to the Dox-treated group. In heart tissues, MDA levels were significantly increased with Dox and decreased with Nec-1 treatment. These results were supported by the histological analysis indicated that Nec-1 reduced doxorubicin-induced cellular injury. Conclusions: In conclusion, our data indicate that Nec-1 ameliorates doxorubicin-induced cardiotoxicity by reducing oxidative stress injury and attenuating apoptosis and necroptosis.en_US
dc.identifier.citationÖzgen, Z.E., Erdinç, M., Kelle, İ., Erdinç, L. ve Nergiz, Y. (2022). Protective effects of necrostatin-1 on doxorubicin-induced cardiotoxicity in rat heart. Human & Experimental Toxicology, 41, 1-8.en_US
dc.identifier.doi10.1177/09603271211066066
dc.identifier.endpage8en_US
dc.identifier.issn0960-3271
dc.identifier.issn1477-0903
dc.identifier.pmid35137609
dc.identifier.scopus2-s2.0-85124286643
dc.identifier.scopusqualityQ2
dc.identifier.startpage1en_US
dc.identifier.urihttps://journals.sagepub.com/doi/10.1177/09603271211066066
dc.identifier.urihttps://hdl.handle.net/11468/11390
dc.identifier.volume41en_US
dc.identifier.wosWOS:000758087100001
dc.identifier.wosqualityQ3
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.institutionauthorÖzgen, Zeynep Erdoğmuş
dc.institutionauthorErdinç, Meral
dc.institutionauthorKelle, İlker
dc.institutionauthorErdinç, Levent
dc.institutionauthorNergiz, Yusuf
dc.language.isoenen_US
dc.publisherSage Publications INC.en_US
dc.relation.ispartofHuman & Experimental Toxicology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectNecroptosisen_US
dc.subjectApoptosisen_US
dc.subjectCaspase-3en_US
dc.subjectBaxen_US
dc.subjectBcl-2en_US
dc.subjectNox-2en_US
dc.titleProtective effects of necrostatin-1 on doxorubicin-induced cardiotoxicity in rat hearten_US
dc.titleProtective effects of necrostatin-1 on doxorubicin-induced cardiotoxicity in rat heart
dc.typeArticleen_US

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