The effects of apocynin on ciprofloxacin-induced oxidative stress-related cardiotoxicity

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dc.contributor.authorOzhan, Onural
dc.contributor.authorColak, Mehmet
dc.contributor.authorYildiz, Azibe
dc.contributor.authorDurhan, Merve
dc.contributor.authorVardi, Nigar
dc.contributor.authorCigremis, Yilmaz
dc.contributor.authorColak, Cemil
dc.date.accessioned2026-04-04T13:34:41Z
dc.date.available2026-04-04T13:34:41Z
dc.date.issued2025
dc.departmentİnönü Üniversitesi
dc.description.abstractCiprofloxacin (CFX), a fluoroquinolone antibiotic, is known to induce oxidative stress-mediated cardiotoxicity. This study investigates the potential protective and therapeutic effects of apocynin (APO), a selective NADPH oxidase (NOX) inhibitor and potent antioxidant, against CFX-induced myocardial injury in rats. Thirty-two male Wistar albino rats were randomly divided into four groups (n = 8). CFX (25 mg/kg, i.p.) was administered twice daily for one week, while APO (20 mg/kg, i.p.) was given once daily for four days either before or after CFX treatment. Hemodynamic parameters (heart rate, systolic, diastolic, and mean blood pressures) and electrocardiographic (ECG) indices (PR, QRS, and QT intervals) were recorded invasively. Histopathological evaluations assessed myocardial inflammation, cardiomyocyte degeneration, and aortic intima-media thickness. Biochemical analyses of cardiac and aortic tissues included measurements of malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) levels. CFX administration significantly elevated cardiac MDA by similar to 45% and decreased SOD and CAT activities by similar to 30-35% (p < 0.05) compared with controls. These alterations were markedly attenuated in APO-treated rats, where antioxidant enzyme activities increased by similar to 25-40% and MDA levels were restored toward normal values (p < 0.05 vs. CFX). APO also shortened the QT interval by similar to 15% and improved systolic pressure by similar to 12% compared with the CFX group (p < 0.05). Histopathological findings confirmed reduced myocardial degeneration and inflammatory infiltration in both APO + CFX and CFX + APO groups. APO effectively ameliorated CFX-induced cardiac oxidative injury by inhibiting NOX2-mediated reactive oxygen species formation and restoring antioxidant defense mechanisms, leading to functional improvement in ECG and hemodynamic parameters. These results suggest that targeted NOX inhibition may represent a practical pharmacological approach to reduce fluoroquinolone-associated cardiotoxicity, warranting further translational investigation.
dc.description.sponsorshipTrkiye Bilimsel ve Teknolojik Arascedil;timath;rma Kurumu [1919B012000052]
dc.description.sponsorshipThe research leading to these results received funding from the Scientific and Technological Research Council of Turkiye (TUB & Idot;TAK) under Grant Agreement No: 1919B012000052.
dc.identifier.doi10.1038/s41598-025-33721-0
dc.identifier.issn2045-2322
dc.identifier.issue1
dc.identifier.pmid41453988
dc.identifier.scopus2-s2.0-105028925607
dc.identifier.scopusqualityN/A
dc.identifier.urihttps://doi.org/10.1038/s41598-025-33721-0
dc.identifier.urihttps://hdl.handle.net/11616/109327
dc.identifier.volume16
dc.identifier.wosWOS:001674051300003
dc.identifier.wosqualityQ1
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherNature Portfolio
dc.relation.ispartofScientific Reports
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.snmzKA_WOS_20250329
dc.subjectCiprofloxacin
dc.subjectApocynin
dc.subjectCardiotoxicity
dc.subjectOxidative stress
dc.subjectRat
dc.titleThe effects of apocynin on ciprofloxacin-induced oxidative stress-related cardiotoxicity
dc.typeArticle

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