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dc.contributor.authorDindaş, Ferhat
dc.contributor.authorGüngör, Hüseyin
dc.contributor.authorEkici, Mehmet
dc.contributor.authorAkokay, Pınar
dc.contributor.authorBayçumendur, Füsun Erhan
dc.contributor.authorDoğduş, Mustafa
dc.contributor.authorYılmaz, Mehmet Birhan
dc.date.accessioned2022-05-11T10:59:53Z
dc.date.available2022-05-11T10:59:53Z
dc.date.issued2021tr
dc.identifier.urihttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8575394/pdf/ajc-25-11-821.pdf
dc.identifier.urihttps://hdl.handle.net/20.500.12418/12789
dc.description.abstractObjective: Doxorubicin (DOX) is a well-known cardiotoxic agent, whereas sacubitril/valsartan (Sac/Val) is an effective treatment option in heart failure. In this study, we aimed to evaluate the effect of Sac/Val on DOX-induced cardiotoxicity in pretreatment mice model. Methods: A total of 24 mice were equally classified into 4 groups; control group, DOX (20 mg/kg; fifth day), Sac/Val (80 mg/kg), and Sac/Val+DOX (Sac/Val was given from day one of the study before doxorubicin administration). Electrocardiography parameters, including durations of QRS, ST, QT, PP segment, and QT/PQ index were measured. Total antioxidant status (TAS), total oxidant status (TOS), tumor necrosis factor-α (TNF-α), interleukin 1β (IL-1β), IL-6, NT-proBNP concentrations, and Caspase 3 activity were evaluated. Results: At the end of the 9-day study duration, QRS, ST, QT intervals, QT/PQ index and TAS, TOS, TNF-α, IL-1β, IL-6 levels were significantly higher in the DOX group than in the control group (p<0.001). Moreover, there were significant differences only in the PP interval when comparing the Sac/Val+DOX and control groups (p<0.001). QRS, ST, QT intervals, and QT/PQ index, TAS, TOS, TNF-α, IL-1β, IL-6 levels were significantly lower in the Sac/Val+ DOX group compared with the DOX group (p<0.001). Furthermore, NT-proBNP levels were lower in the Sac/Val+DOX group compared with the DOX group along with less Caspase 3 apoptosis. Conclusion: Sac/Val seems to be cardioprotective against DOX-induced cardiotoxicity in pretreatment mice model. These findings can be attributed to the antiarrhythmic, anti-inflammatory, antioxidant, and antiapoptotic effects of Sac/Val as shown in this studytr
dc.language.isoengtr
dc.publisherAVEStr
dc.relation.isversionofhttps://dx.doi.org/10.5152/AnatolJCardiol.2021.356tr
dc.rightsinfo:eu-repo/semantics/openAccesstr
dc.subjectsacubitril, valsartan, doxorubicin, cardiotoxicity, heart failuretr
dc.titleAngiotensin receptor-neprilysin inhibition by sacubitril/valsartan attenuates doxorubicin induced cardiotoxicity in a pretreatment mice model by interfering with oxidative stress, inflammation, and Caspase 3 apoptotic pathwaytr
dc.typearticletr
dc.relation.journalThe Anatolian Journal of Cardiologytr
dc.contributor.departmentVeteriner Fakültesitr
dc.relation.publicationcategoryUluslararası Hakemli Dergide Makale - Kurum Öğretim Elemanıtr


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