The effect of adenosine triphosphate on sunitinib-induced cardiac injury in rats

ArticleAçık Erişim

Özet

In this study, we aimed to show the effect of adenosine 5′-triphosphate (ATP) on sunitinib-induced cardiac injury in rats. The rats (n = 30) were divided equally into three groups as sunitinib group (SG), sunitinib plus ATP group (SAG), and healthy group (HG); 2 mg/kg ATP was injected intraperitoneally (ip) to the SAG group. Same volume normal saline as solvent was administered ip to the other two groups. After 1 h, 25 mg/kg sunitinib was applied orally via catheter to stomach in the SAG and SG groups. This procedure was repeated once daily for 5 weeks. At the end of this period, all animals were sacrificed and their cardiac tissue was removed. Malondialdehyde (MDA), total glutathione (tGSH), tumor necrosis factor α (TNF-α), and nuclear factor κB (NF-κB) levels in rats’ cardiac tissues and troponin I (Tp-I) levels in rats’ blood samples were evaluated. Histopathological analysis was also performed in cardiac tissues of the animals. MDA, TNF-α, NF-κB, and Tp-I levels were higher in the SG group compared to the SAG and HG groups (p < 0.001). tGSH levels of the SG group were lower than the SAG and HG groups (p < 0.001). The structure and morphology of cardiac muscle fibers and blood vessels were normal in the control group. In the SG group, obvious cardiac muscle tissue damage with dilated myofibers, locally atrophic myofibers, and congested blood vessels were observed. In the SAG group, marked amelioration in these findings was observed. We showed this for the first time that ATP administration exerts a protective effect against cardiac effects of sunitinib. © The Author(s) 2020.

Anahtar Kelimeler

RDL Kalıcı Bağlantı (PID)
https://rdlopen.rawdatalibrary.net/r/ebyu/13701Resmi atıflarda kullanılan kalıcı adres
DOI
https://doi.org/10.1177/0960327120909874Yayıncı resmi DOI adresi
Tam Kayıt
AlanDeğerDil
dc.contributor.authorAldemir, M.N.
dc.contributor.authorSimsek, M.
dc.contributor.authorKara, A.V.
dc.contributor.authorOzcicek, F.
dc.contributor.authorMammadov, R.
dc.contributor.authorYazıcı, G.N.
dc.contributor.authorSunar, M.
dc.contributor.authorCoskun, R.
dc.contributor.authorGulaboglu, M.
dc.contributor.authorSuleyman, H.
dc.date.accessioned2026-10-18T20:28:31.650559159Z
dc.date.available2026-10-18T20:28:31.650559159Z
dc.date.issued2020
dc.description.abstractIn this study, we aimed to show the effect of adenosine 5′-triphosphate (ATP) on sunitinib-induced cardiac injury in rats. The rats (n = 30) were divided equally into three groups as sunitinib group (SG), sunitinib plus ATP group (SAG), and healthy group (HG); 2 mg/kg ATP was injected intraperitoneally (ip) to the SAG group. Same volume normal saline as solvent was administered ip to the other two groups. After 1 h, 25 mg/kg sunitinib was applied orally via catheter to stomach in the SAG and SG groups. This procedure was repeated once daily for 5 weeks. At the end of this period, all animals were sacrificed and their cardiac tissue was removed. Malondialdehyde (MDA), total glutathione (tGSH), tumor necrosis factor α (TNF-α), and nuclear factor κB (NF-κB) levels in rats’ cardiac tissues and troponin I (Tp-I) levels in rats’ blood samples were evaluated. Histopathological analysis was also performed in cardiac tissues of the animals. MDA, TNF-α, NF-κB, and Tp-I levels were higher in the SG group compared to the SAG and HG groups (p < 0.001). tGSH levels of the SG group were lower than the SAG and HG groups (p < 0.001). The structure and morphology of cardiac muscle fibers and blood vessels were normal in the control group. In the SG group, obvious cardiac muscle tissue damage with dilated myofibers, locally atrophic myofibers, and congested blood vessels were observed. In the SAG group, marked amelioration in these findings was observed. We showed this for the first time that ATP administration exerts a protective effect against cardiac effects of sunitinib. © The Author(s) 2020.
dc.identifier.doi10.1177/0960327120909874
dc.identifier.eissn1477-0903
dc.identifier.endpage1053
dc.identifier.issn0960-3271
dc.identifier.issue8
dc.identifier.pmid32131635
dc.identifier.scopus2-s2.0-85081677758
dc.identifier.startpage1046
dc.identifier.urihttps://rdlopen.rawdatalibrary.net/r/ebyu/13701
dc.identifier.volume39
dc.identifier.wosWOS:000523178100001
dc.language.isoen
dc.publisherSAGE Publications Ltd
dc.relation.ispartofHuman and Experimental Toxicology
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectAdenosine triphosphate
dc.subjectcardiotoxicity
dc.subjectsunitinib
dc.subjectAnimals
dc.subjectAntineoplastic Agents
dc.subjectCardiotonic Agents
dc.subjectCardiotoxins
dc.subjectGlutathione
dc.subjectMale
dc.subjectMalondialdehyde
dc.subjectMyocardium
dc.subjectNF-kappa B
dc.subjectProtein Kinase Inhibitors
dc.subjectRats, Wistar
dc.subjectTroponin I
dc.subjectTumor Necrosis Factor-alpha
dc.subjectimmunoglobulin enhancer binding protein
dc.subjectmalonaldehyde
dc.subjectsodium chloride
dc.subjecttumor necrosis factor
dc.subjectantineoplastic agent
dc.subjectcardiotonic agent
dc.subjectcardiotoxin
dc.subjectprotein kinase inhibitor
dc.subjectanimal cell
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectanimal tissue
dc.subjectArticle
dc.subjectatrophy
dc.titleThe effect of adenosine triphosphate on sunitinib-induced cardiac injury in rats
dc.typeArticle
dspace.entity.typePublication
rdl.citation.scopus16
rdl.citation.wos17
rdl.departmentDepartment of Nephrology, Faculty of Medicine, Erzincan University, Erzincan, Turkey. | Department of Internal Medicine, Faculty of Medicine, Erzincan University, Erzincan, Turkey. | Department Pharmacology, Faculty of Medicine, Erzincan University, Erzincan, Turkey. | Department of Histology and Embryology, Faculty of Medicine, Erzincan University, Erzincan, Turkey. | Department of Anatomy, Faculty of Medicine, Erzincan University, Erzincan, Turkey. | Department of Cardiology, Faculty of Medicine, Erzincan University, Erzincan, Turkey. | Department of Pharmacology, Faculty of Medicine, Erzincan University, Erzincan, Turkey.
rdl.source.indexSCOPUS
rdl.source.indexWOS
rdl.source.indexPUBMED
rdl.wos.indexScience Citation Index Expanded (SCI-EXPANDED)