N-acetyl cysteine amide mitigates oxidative stress and apoptosis in a rat model of renal ischemia-reperfusion injury

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dc.contributor.authorOzhan, Onural
dc.contributor.authorEkici, Cihan
dc.contributor.authorAtes, Burhan
dc.contributor.authorYildiz, Azibe
dc.contributor.authorBalcioglu, Sevgi
dc.contributor.authorVardi, Nigar
dc.contributor.authorParlakpinar, Hakan
dc.date.accessioned2026-04-04T13:34:40Z
dc.date.available2026-04-04T13:34:40Z
dc.date.issued2026
dc.departmentİnönü Üniversitesi
dc.description.abstractRenal ischemia-reperfusion (IR) injury is a major cause of acute kidney injury, in which oxidative stress (OS) and apoptosis play central roles. N-acetyl cysteine amide (NACA), a lipophilic derivative of N-acetylcysteine, exhibits improved cellular penetration and antioxidant activity. This study investigated the renoprotective effects of NACA in a rat model of renal IR injury. Twenty-eight female Wistar albino rats were randomized into four groups (n = 7): Control, IR, NACA + IR (100 mg/kg i.p., 30 min before ischemia), and IR + NACA (100 mg/kg i.p., immediately after ischemia). Following right nephrectomy, the left renal pedicle was clamped for 60 min and reperfused for 24 h. Serum renal function markers, kidney OS parameters, histopathological injury, and caspase-3 immunoreactivity were evaluated. Renal IR injury significantly increased serum blood urea nitrogen and creatinine levels and induced histopathological damage characterized by tubular dilatation, cast formation, and degeneration. Catalase (CAT) and superoxide dismutase (SOD) activities were significantly altered; malondialdehyde increased after IR and was reduced by NACA pretreatment, whereas myeloperoxidase and total glutathione did not differ significantly among groups. NACA pretreatment attenuated inflammatory cell infiltration, tubular dilatation, and caspase-3 immunoreactivity, while partially restoring CAT and SOD activity. Post-ischemic NACA administration was less effective, particularly in reducing apoptosis and inflammatory infiltration. NACA confers partial renoprotection against renal IR injury, with pretreatment providing superior efficacy. These findings highlight the importance of antioxidant timing and suggest NACA as a potential prophylactic strategy when renal ischemia is predictable.
dc.description.sponsorshipTrkiye Bilimsel ve Teknolojik Arascedil;timath;rma Kurumu [2209a]
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:1919B011503666.
dc.identifier.doi10.1038/s41598-026-37274-8
dc.identifier.issn2045-2322
dc.identifier.issue1
dc.identifier.pmid41593161
dc.identifier.scopus2-s2.0-105030050637
dc.identifier.scopusqualityN/A
dc.identifier.urihttps://doi.org/10.1038/s41598-026-37274-8
dc.identifier.urihttps://hdl.handle.net/11616/109317
dc.identifier.volume16
dc.identifier.wosWOS:001691512400002
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.subjectN-acetyl cysteine amide
dc.subjectIschemia-reperfusion injury
dc.subjectOxidative stress
dc.subjectApoptosis
dc.subjectKidney
dc.subjectRat
dc.titleN-acetyl cysteine amide mitigates oxidative stress and apoptosis in a rat model of renal ischemia-reperfusion injury
dc.typeArticle

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