Angiotensin 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 pathway

Basit Öğe Kaydı
dc.contributor.authorDindaş, Ferhat
dc.contributor.authorGüngör, Hüseyin
dc.contributor.authorEkici, Mehmet
dc.contributor.authorAkokay, Pınar
dc.contributor.authorErhan, Füsun
dc.contributor.authorDogdus, Mustafa
dc.contributor.authorYılmaz, Mehmet Birhan
dc.date.accessioned2024-10-26T17:42:54Z
dc.date.available2024-10-26T17:42:54Z
dc.date.issued2021
dc.departmentSivas Cumhuriyet Üniversitesi
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-? (TNF-?), interleukin 1? (IL-1?), 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-?, IL-1?, 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-?, IL-1?, 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 study.
dc.identifier.doi10.5152/AnatolJCardiol.2021.356
dc.identifier.endpage828
dc.identifier.issn2149-2263
dc.identifier.issn2149-2271
dc.identifier.issue11
dc.identifier.startpage821
dc.identifier.trdizinid487683
dc.identifier.urihttps://doi.org/10.5152/AnatolJCardiol.2021.356
dc.identifier.urihttps://search.trdizin.gov.tr/tr/yayin/detay/487683
dc.identifier.urihttps://hdl.handle.net/20.500.12418/24876
dc.identifier.volume25
dc.indekslendigikaynakTR-Dizin
dc.language.isoen
dc.relation.ispartofThe Anatolian Journal of Cardiology
dc.relation.publicationcategoryMakale - Ulusal Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
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 pathway
dc.typeArticle

Dosyalar

Koleksiyon

TR-Dizin İndeksli Yayınlar Koleksiyonu