Investigation of cardioprotective effect of lercanidipine on doxorubicin-induced cardiotoxicity

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dc.authorid0000-0002-2249-4668
dc.authorid0000-0001-6835-4436
dc.contributor.authorKarakuyu, Nasif Fatih
dc.contributor.authorSavran, Mehtap
dc.contributor.authorCandan, Ibrahim Aydin
dc.contributor.authorBuyukbayram, Halil Ibrahim
dc.contributor.authorErzurumlu, Yalcin
dc.date.accessioned2026-01-24T12:30:52Z
dc.date.available2026-01-24T12:30:52Z
dc.date.issued2023
dc.departmentAlanya Alaaddin Keykubat Üniversitesi
dc.description.abstractAlthough doxorubicin (DOX) is an effective anti-neoplastic drug for many types of cancer, particularly dose-related cardiotoxicity limits the use of the drug. In this study, it was aimed to investigate the protective effect of lercanidipine (LRD) against DOX-induced cardiotoxicity. In our study, 40 Wistar albino female rats were randomly divided into 5 groups as control, DOX, LRD 0.5 (DOX + 0.5 mg/kg LRD), LRD 1 (DOX + 1 mg/kg LRD), and LRD 2 (DOX + 2 mg/kg LRD). At the end of the experiment, the rats were sacrificed, and their blood, heart, and endothelial tissues were examined biochemically, histopathologically, immunohistochemically, and genetically. According to our findings, necrosis, tumor necrosis factor alpha activity, vascular endothelial growth factor activity, and oxidative stress were increased in the heart tissues of the DOX group. In addition, DOX treatment caused the deteriorations in biochemical parameters, and levels of autophagy-related proteins, Atg5, Beclin1, and LC3-I/II were detected. Significant dose-related improvements in these findings were observed with LRD treatment. Besides, Atg5, LC3-I/II, and Beclin1 levels evaluated by western blot revealed that LRD exerts a tissue protective effect by regulating autophagy in endothelial tissue. LRD treatment, which is a new-generation calcium channel blocker, showed antioxidant, anti-inflammatory, and anti-apoptotic properties in heart and endothelial tissue in a dose-dependent manner and also showed protective activity by regulating autophagy in endothelial tissue. With studies evaluating these mechanisms in more detail, the protective effects of LRD will be revealed more clearly.
dc.description.sponsorshipScientific Research Project Unit of Suleyman Demirel University [TDK-20228639]
dc.description.sponsorshipThis study was supported by the Scientific Research Project Unit of Suleyman Demirel University (project code: TDK-2022-8639).
dc.identifier.doi10.1007/s00210-023-02566-7
dc.identifier.endpage3645
dc.identifier.issn0028-1298
dc.identifier.issn1432-1912
dc.identifier.issue12
dc.identifier.pmid37284897
dc.identifier.scopus2-s2.0-85161314019
dc.identifier.scopusqualityQ2
dc.identifier.startpage3635
dc.identifier.urihttps://doi.org/10.1007/s00210-023-02566-7
dc.identifier.urihttps://hdl.handle.net/20.500.12868/5499
dc.identifier.volume396
dc.identifier.wosWOS:001004095000003
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherSpringer
dc.relation.ispartofNaunyn-Schmiedebergs Archives of Pharmacology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.snmzKA_WoS_20260121
dc.subjectAutophagy
dc.subjectCardioprotective
dc.subjectDoxorubicin
dc.subjectLercanidipine
dc.titleInvestigation of cardioprotective effect of lercanidipine on doxorubicin-induced cardiotoxicity
dc.typeArticle

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