Alamandine alleviates methotrexate-induced nephrotoxicity in rats by targeting oxidative stress and inflammation

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dc.contributor.authorYıldız, Azibe
dc.contributor.authorAras, Muhammed Yasir
dc.contributor.authorGunata, Mehmet
dc.contributor.authorDurhan, Merve
dc.contributor.authorPolat, Seyhan
dc.contributor.authorParlakpınar, Hakan
dc.contributor.authorCigremis, Yilmaz
dc.date.accessioned2024-08-04T19:42:43Z
dc.date.available2024-08-04T19:42:43Z
dc.date.issued2023
dc.departmentİnönü Üniversitesien_US
dc.description.abstractAim: Nephrotoxicity due to the use of methotrexate (Mtx) is one of the most important problems associated with chemotherapy. Oxidative stress and inflammation are the major pathomechanisms of Mtx-induced nephrotoxicity. Alamandine (Ala), a new member of the renin-angiotensin system (RAS), is an important peptide with antioxidant and antiinflammatory capacities. In this study, it was investigated whether Ala ameliorates Mtxinduced kidney damage by reducing oxidative stress and inflammation. Materials and Methods: Male Wistar albino rats were assigned into three groups: control group, Mtx group, and Mtx+Ala group. At the end of the experiment, kidney tissues were quickly removed. Glutathione (GSH) and malondialdehyde (MDA) levels were measured to determine the oxidative state in kidney tissues. In addition, tissue samples were assessed as histopathological and immunohistochemical for heat shock protein 60 (HSP60), caspase-3, tumor necrosis factor-? (TNF-?), and receptor-interacting protein kinase-3 (RIPK3). Results: Mtx treatment resulted in reduced GSH content, elevated MDA level, increased heat shock protein 60 (HSP60), and caspase-3 expression. These changes in kidney tissues of rats treated with Mtx triggered oxidative stress characterized by apoptosis and kidney damage. Mtx also markedly increased the expression of TNF-?, an inflammation marker, and RIPK3, a marker of necroptosis. However, Ala administration significantly alleviated Mtx-induced kidney damage by reducing apoptosis and necroptosis by suppressing oxidative stress and inflammation. Conclusion: Taken together, our results support that Ala treatment can serve as a new and promising therapeutic strategy against Mtx-induced nephrotoxicity.en_US
dc.identifier.doi10.5455/annalsmedres.2023.06.128
dc.identifier.endpage904en_US
dc.identifier.issn2636-7688
dc.identifier.issue8en_US
dc.identifier.startpage899en_US
dc.identifier.trdizinid1205786en_US
dc.identifier.urihttps://doi.org/10.5455/annalsmedres.2023.06.128
dc.identifier.urihttps://search.trdizin.gov.tr/yayin/detay/1205786
dc.identifier.urihttps://hdl.handle.net/11616/88622
dc.identifier.volume30en_US
dc.indekslendigikaynakTR-Dizinen_US
dc.language.isoenen_US
dc.relation.ispartofAnnals of Medical Researchen_US
dc.relation.publicationcategoryMakale - Ulusal Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.titleAlamandine alleviates methotrexate-induced nephrotoxicity in rats by targeting oxidative stress and inflammationen_US
dc.typeArticleen_US

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