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dc.contributor.authorSakul, Arzu
dc.contributor.authorOzansoy, Mehmet
dc.contributor.authorElibol, Birsen
dc.contributor.authorAyla, Şule
dc.contributor.authorGünal, Mehmet Yalçın
dc.contributor.authorYozgat, Yasemin
dc.contributor.authorKılıç, Ülkan
dc.date.accessioned2021-02-19T21:29:05Z
dc.date.available2021-02-19T21:29:05Z
dc.date.issued2019
dc.identifier.issn1300-0152
dc.identifier.issn1303-6092
dc.identifier.urihttps://doi.org/10.3906/biy-1902-77
dc.identifier.urihttps://app.trdizin.gov.tr/makale/TXpNMk1EUXlNZz09
dc.identifier.urihttps://hdl.handle.net/20.500.12868/962
dc.description.abstractThe clinical use of cisplatin, which is a first-line anticancer agent, is highly restricted due to its adverse effects on kidneys that lead to nephrotoxicity. Therefore, some potential reno-protective substances have been used in combination with cisplatin to cope with nephrotoxicity. Due to its high antitumor activity and oxygen-carrying capacity, we investigated the molecular effects of squalene against cisplatin-induced oxidative stress and kidney damage in mice. Single dose of cisplatin (7 mg/kg) was given to male Balb/c mice. Squalene (100 mg/kg/day) was administered orogastrically to mice for 10 days. Following sacrification, molecular alterations were investigated as analysis of the levels of oxidative stress index (OSI), inflammatory cytokines and cell survival-related proteins in addition to histopathological examinations in mice kidney tissue. The level OSI and Interferon-gamma (IFN-?) decreased in the cisplatin and squalene cotreated mice compared to cisplatin-treated mice. Squalene treatment also increased the activation of protein kinase B (AKT). Furthermore, cisplatin-induced inactivation of mammalian target of rapamycin (mTOR) and histopathological damages were reversed by squalene. It may be suggested that squalene ameliorated the cisplatin-induced histopathological damages in the kidneyen_US
dc.language.isoengen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectBiyolojien_US
dc.titleSqualene attenuates the oxidative stress and activates AKT/mTOR pathway against cisplatin-induced kidney damage in miceen_US
dc.typearticleen_US
dc.contributor.departmentALKÜen_US
dc.contributor.institutionauthor0-belirlenecek
dc.identifier.doi10.3906/biy-1902-77
dc.identifier.volume43en_US
dc.identifier.issue3en_US
dc.identifier.startpage179en_US
dc.identifier.endpage188en_US
dc.relation.journalTurkish Journal of Biologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US


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