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dc.contributor.authorKılıç, Ülkan
dc.contributor.authorKılıç, Ertuğrul
dc.contributor.authorTuzcu, Zeynep
dc.contributor.authorTuzcu, Mehmet
dc.contributor.authorÖzercan, İbrahim
dc.contributor.authorYılmaz, Ökkeş
dc.contributor.authorŞahin, Fikrettin
dc.contributor.authorŞahin, Kazım
dc.date.accessioned10.07.201910:49:13
dc.date.accessioned2019-07-10T20:02:10Z
dc.date.available10.07.201910:49:13
dc.date.available2019-07-10T20:02:10Z
dc.date.issued2013en_US
dc.identifier.citationKılıç, Ü., Kılıç, E., Tuzcu, Z., Tuzcu, M., Özercan, İ., Yılmaz, Ö. ... Şahin, K. (2013). Melatonin suppresses cisplatin-induced nephrotoxicity via activation of Nrf-2/HO-1 pathway. Nutrition & Metabolism, 10(1). https://dx.doi.org/10.1186/1743-7075-10-7en_US
dc.identifier.issn1743-7075
dc.identifier.urihttps://dx.doi.org/10.1186/1743-7075-10-7
dc.identifier.urihttps://hdl.handle.net/20.500.12511/3572
dc.descriptionWOS: 000314541600001en_US
dc.descriptionPubMed ID: 23311701en_US
dc.description.abstractBackground: Cisplatin, one of the most effective and potent anticancer drugs, is used in the treatment of a wide variety of both pediatric and adult malignancies. However, the chemotherapeutic use of cisplatin is limited by its serious side-effects such as nephrotoxicity and ototoxicity. Cisplatin chemotherapy induces a reduction in the antioxidant status, leading to a failure of the antioxidant defense against free-radical damage generated by antitumor drugs. Cisplatin-induced oxidative stress in the kidney was partially prevented by antioxidant treatments using superoxide dismutase, glutathione, selenium and flavonoids. Melatonin and its metabolites possess free-radical scavenging activity and it has been shown that they protect against cisplatin toxicity. However, the mechanism of the protective effects of melatonin against cisplatin-induced nephrotoxicity is still essentially unknown. We therefore designed this study to investigate the underlying mechanism of the protective effect of melatonin against cisplatin-induced renal damage in a rat nephrotoxicity model in vivo. Methods: Twenty eight 8-week-old male Wistar rats were divided into four groups of control, melatonin treatment (4 mg/kg b.w i.p. for 10 days), cisplatin treatment (7 mg/kg b.w., i.p.) and melatonin and cisplatin combination treatment. Serum urea nitrogen (urea-N) and creatinine levels were measured. Histopathological changes were evaluated. In addition, we analyzed the expression levels of HO-1, Nrf2, NF-kappa B and AP-1 in Western blot analysis. Results: Both serum creatinine and urea nitrogen increased significantly following cisplatin administration alone; these values decreased significantly with melatonin co-treatment of cisplatin-treated rats. Histological analysis showed that cisplatin caused damage in the proximal tubular cells in the kidneys of cisplatin-treated rats; these changes were reversed by melatonin co-treatment. Upon Western blot analysis, melatonin treatment increased Nrf2 accumulation in the nuclear fraction, and increased the expression of HO-1 in the cytosolic fraction as compared to the cisplatin-treated rats. Expressions of NF-kappa B p65 and AP-1 were increased significantly in the kidneys of rats treated with cisplatin compared with the expression in the kidneys from the control, melatonin-only-treated and melatonin co-treated rats. Conclusion: Our present data suggest that melatonin attenuates cisplatin-induced nephrotoxicity possibly by modulating Nrf2/HO-1 signaling.en_US
dc.description.sponsorshipEMBO (European Molecular Biology Organization) installation grant; Turkish Academy of Sciences (TUBA)en_US
dc.description.sponsorshipThis work was supported by EMBO (European Molecular Biology Organization) installation grant and The Turkish Academy of Sciences (TUBA).en_US
dc.language.isoengen_US
dc.publisherBiomed Central Ltden_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectNephrotoxicityen_US
dc.subjectNrf2/HO-1 signalingen_US
dc.subjectMelatoninen_US
dc.subjectOxidative stressen_US
dc.titleMelatonin suppresses cisplatin-induced nephrotoxicity via activation of Nrf-2/HO-1 pathwayen_US
dc.typearticleen_US
dc.relation.ispartofNutrition & Metabolismen_US
dc.departmentİstanbul Medipol Üniversitesi, Uluslararası Tıp Fakültesi, Temel Tıp Bilimleri Bölümü, Fizyoloji Ana Bilim Dalıen_US
dc.authorid0000-0001-6494-8923en_US
dc.identifier.volume10en_US
dc.identifier.issue1en_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.identifier.doi10.1186/1743-7075-10-7en_US
dc.identifier.wosqualityQ2en_US
dc.identifier.scopusqualityQ1en_US


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