Protective effect of betulinic acid administration on kidney damage in acetaminophen-induced nephrotoxicity model

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dc.authorid0000-0002-2223-1331
dc.authorid0000-0002-8063-4972
dc.authorid0000-0002-4446-0848
dc.authorid0000-0003-0819-8843
dc.authorid0000-0002-1740-8657
dc.authorid0000-0003-1398-7046
dc.authorid0000-0003-3877-7686
dc.contributor.authorDokumacıoğlu, Eda
dc.contributor.authorİskender, Hatice
dc.contributor.authorHayırlı, Armağan
dc.contributor.authorYenice, Güler
dc.contributor.authorTerim Kapakin, Kübra Asena
dc.contributor.authorBolat, İsmail
dc.contributor.authorManavoğlu Kirman, Esra
dc.date.accessioned2025-10-16T08:06:41Z
dc.date.available2025-10-16T08:06:41Z
dc.date.issued2023
dc.departmentAÇÜ, Sağlık Bilimleri Fakültesi, Beslenme ve Diyetetik Bölümü
dc.description.abstractBackground: Acetaminophen (APAP) is the most widely used analgesic drug worldwide, but it may induce renal toxicity. Betulinic acid (BA) ameliorates the oxidative stress and inflammatory response to renal damage. The present study aimed to investigate the potential protective effects of BA treatment through an experimental kidney damage rat model administered with APAP. Methods: Sprague-Dawley male rats were randomly divided into four groups: control, BA (25 mg/kg for 15 days), APAP (1 g/kg), and APAP + BA groups. BA was administered via oral gavage at a dose of 25 mg/kg for 15 days. APAP was dissolved in hot saline and administered on the last day to produce nephrotoxicity via a single oral gavage at a dose of 1 g/kg. Kidney tissue samples were analyzed for human cartilage glycoprotein 39 (YKL-40), kidney injury molecule 1 (KIM-1), interleukin 18 (IL-18), superoxide dismutase (SOD), and malondialdehyde (MDA). Data were subjected to one-way analysis of variance and the Wilcoxon rank-sum test Results: Renal tissue YKL-40, KIM-1, IL-18, and MDA levels in the APAP group were significantly higher than those in the control group (p < 0.05). The BA treatment completely restored renal KIM-1, YKL-40, and MDA levels and partially restored renal IL-18 and SOD levels in the rats subjected to renal damage induction (p < 0.05). The intertubular regions of rats administered with APAP had degeneration, necrosis, and infiltration of inflammatory cells and were immunopositive for IL-1 beta and 8-hydroxy-2 & PRIME;-deoxyguanosine. Conclusions: BA can be used in the prevention and replacement treatment of nephrotoxicity due to its inhibitory properties in multiple pathways and powerful antioxidant effects.
dc.identifier.doi10.7454/msk.v27i1.1438
dc.identifier.endpage67
dc.identifier.issn2356-3664
dc.identifier.issue1
dc.identifier.startpage59
dc.identifier.urihttps://hdl.handle.net/11494/6113
dc.identifier.volume27
dc.identifier.wosWOS:001031786400008
dc.identifier.wosqualityQ4
dc.indekslendigikaynakWeb of Science
dc.institutionauthorDokumacıoğlu, Eda
dc.institutionauthorİskender, Hatice
dc.institutionauthorid0000-0002-2223-1331
dc.institutionauthorid0000-0002-8063-4972
dc.language.isoen
dc.publisherUNIV INDONESIA
dc.relation.ispartofMAKARA JOURNAL OF HEALTH RESEARCH
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectAcetaminophen
dc.subjectBetulinic acid
dc.subjectInterleukin 18
dc.subjectKidney injury molecule 1
dc.subjectMalondialdehyde
dc.subjectSuperoxide dismutase
dc.titleProtective effect of betulinic acid administration on kidney damage in acetaminophen-induced nephrotoxicity model
dc.typeArticle

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