Eucalyptol regulates Nrf2 and NF-kB signaling and alleviates gentamicin-induced kidney injury in rats by downregulating oxidative stress, oxidative DNA damage, inflammation, and apoptosis

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dc.authoridKIRGIZ, Omer/0000-0002-0222-1363
dc.authoridKARATAS, Ozhan/0000-0002-2778-8059
dc.authoridAkcakavak, Gokhan/0000-0001-5949-4752
dc.authoridTuzcu, Mehmet/0000-0003-3118-1054
dc.authoridCELIK, Zeynep/0000-0002-9667-5728
dc.authoridKazak, Filiz/0000-0002-9065-394X
dc.contributor.authorAkcakavak, Gokhan
dc.contributor.authorKazak, Filiz
dc.contributor.authorKaratas, Ozhan
dc.contributor.authorAlakus, Halil
dc.contributor.authorAlakus, Ibrahim
dc.contributor.authorKirgiz, Omer
dc.contributor.authorCelik, Zeynep
dc.date.accessioned2024-10-26T18:09:19Z
dc.date.available2024-10-26T18:09:19Z
dc.date.issued2024
dc.departmentSivas Cumhuriyet Üniversitesi
dc.description.abstractGentamicin, an aminoglycoside antibiotic, is nowadays widely used in the treatment of gram-negative microorganisms. The antimicrobial, anti-inflammatory, and antioxidant activities of eucalyptol, a type of saturated monoterpene, have been reported in many studies. The aim of this study was to examine the possible effects of eucalyptol on gentamicin-induced renal toxicity. A total of 32 rats were divided into 4 groups; Control (C), Eucalyptol (EUC), Gentamicin (GEN), and Gentamicin + Eucalyptol (GEN + EUC). In order to induce renal toxicity, 100 mg/kg gentamicin was administered intraperitoneally (i.p.) for 10 consecutive days in the GEN and GEN + EUC groups. EUC and GEN + EUC groups were given 100 mg/kg orally of eucalyptol for 10 consecutive days. Afterwards, rats were euthanized and samples were taken and subjected to histopathological, biochemical, immunohistochemical, and real-time PCR examinations. The blood urea nitrogen (BUN) and creatinine (CRE) levels were significantly decreased in the GEN + EUC group (0.76 and 0.69-fold, respectively) compared to the GEN group. The glutathione peroxidase (GPx) and catalase (CAT) activities were significantly increased in the GEN + EUC group (1.35 and 2.67-fold, respectively) compared to the GEN group. In GEN group, Nuclear factor kappa B (NF-kB), Interleukin 1-beta (IL-1 beta), Inducible nitric oxide synthase (iNOS), Tumor necrosis factor-alpha (TNF-alpha), Caspase-3, 8-Hydroxy-2 '-deoxyguanosine (8-OHdG) and Nuclear factor erythroid 2-related factor (Nrf2) expression levels were found to be quite irregular. GEN + EUC group decreased the expressions of NF-kB, IL-1 beta, iNOS, TNF-alpha, Caspase-3, and 8-OHdG (0.55, 0.67, 0.54, 0.54, 0.63 and 0.67 fold, respectively), while it caused increased expression of Nrf2 (3.1 fold). In addition, eucalyptol treatment ameliorated the histopathological changes that occurred with gentamicin. The results of our study show that eucalyptol has anti-inflammatory, antioxidative, antiapoptotic, nephroprotective, and curative effects on gentamicin-induced nephrotoxicity.
dc.identifier.doi10.1080/15376516.2023.2297234
dc.identifier.endpage422
dc.identifier.issn1537-6516
dc.identifier.issn1537-6524
dc.identifier.issue4
dc.identifier.pmid38115227
dc.identifier.scopus2-s2.0-85180830477
dc.identifier.scopusqualityQ2
dc.identifier.startpage413
dc.identifier.urihttps://doi.org/10.1080/15376516.2023.2297234
dc.identifier.urihttps://hdl.handle.net/20.500.12418/30064
dc.identifier.volume34
dc.identifier.wosWOS:001132161200001
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherTaylor & Francis Ltd
dc.relation.ispartofToxicology Mechanisms and Methods
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectGentamicin
dc.subjecteucalyptol
dc.subjectnephrotoxicity
dc.subjectoxidative stress
dc.subjectapoptosis
dc.subjectinflammation
dc.titleEucalyptol regulates Nrf2 and NF-kB signaling and alleviates gentamicin-induced kidney injury in rats by downregulating oxidative stress, oxidative DNA damage, inflammation, and apoptosis
dc.typeArticle

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