Protective effect of chelerythrine on gentamicin-induced nephrotoxicity

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dc.authoridPolat, Alaadin/0000-0002-6920-3856
dc.authoridAcet, Ahmet/0000-0003-1131-1878
dc.authoridParlakpinar, Hakan/0000-0001-9497-3468
dc.authoridParlakpınar, Hakan/0000-0001-9497-3468
dc.authoridVardı, Nigar/0000-0003-0576-1696
dc.authoridbay karabulut, aysun/0000-0002-7873-2805
dc.authorwosidPolat, Alaadin/AAA-7171-2021
dc.authorwosidAcet, Ahmet/AAB-3273-2021
dc.authorwosidParlakpinar, Hakan/V-6637-2019
dc.authorwosidKAVAKLI, AHMET/V-8005-2018
dc.authorwosidParlakpınar, Hakan/T-6517-2018
dc.authorwosidVardı, Nigar/C-9549-2018
dc.authorwosidbay karabulut, aysun/HJP-0995-2023
dc.contributor.authorParlakpinar, H
dc.contributor.authorTasdemir, S
dc.contributor.authorPolat, A
dc.contributor.authorBay-Karabulut, A
dc.contributor.authorVardi, N
dc.contributor.authorUcar, M
dc.contributor.authorYanilmaz, M
dc.date.accessioned2024-08-04T20:15:13Z
dc.date.available2024-08-04T20:15:13Z
dc.date.issued2006
dc.departmentİnönü Üniversitesien_US
dc.description.abstractDespite their beneficial effects, aminoglycosides including gentamicin (GEN) have considerable nephrotoxic side-effects. The toxicity of GEN at the level of the kidney seems to relate to the generation of reactive oxygen species (ROS). ROS have been reported to be involved in the activation of protein kinase C (PKC). The unique structural aspects of PKC cause it to function as a sensor for oxidative stress. It seems likely that the increased NAD(P)H oxidase-derived superoxide (O-2) production is at least in part mediated by PKC. We investigated the effects of chelerythrine, a commonly used PKC inhibitor, on GEN-induced changes of renal malondialdehyde (MDA), nitric oxide (NO) generation, catalase (CAT), superoxide disniutase (SOD), glutathione peroxidase (GSH-Px) activities, glutathione (GSH) content, and serum creatinine (Cr), blood urea nitrogen (BUN) levels. Morphological changes in the kidney were also examined. GEN administration to control rats increased MDA and NO generation but decreased CAT, SOD and GSH-Px activities, and GSH content. Chelerythrine administration with GEN caused significantly decreased MDA, NO generation and increased CAT, SOD and GSH-Px activities, and GSH content when compared with GEN alone. Chelerythrine also significantly decreased serum Cr and BUN levels. Morphological changes in the kidney including tubular necrosis were evaluated qualitatively. Both biochemical findings and histopathological evidence showed that administration of chelerythrine reduced the GEN-induced kidney damage. We propose that chelerythrine acts in the kidney as a potent scavenger of free radicals to prevent the toxic effects of GEN via the inhibition of a PKC pathway. Copyright (c) 2004 John Wiley & Sons, Ltd.en_US
dc.identifier.doi10.1002/cbf.1182
dc.identifier.endpage48en_US
dc.identifier.issn0263-6484
dc.identifier.issn1099-0844
dc.identifier.issue1en_US
dc.identifier.pmid15584091en_US
dc.identifier.scopus2-s2.0-31644448165en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage41en_US
dc.identifier.urihttps://doi.org/10.1002/cbf.1182
dc.identifier.urihttps://hdl.handle.net/11616/94254
dc.identifier.volume24en_US
dc.identifier.wosWOS:000235145200005en_US
dc.identifier.wosqualityQ4en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherWileyen_US
dc.relation.ispartofCell Biochemistry and Functionen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectgentamicinen_US
dc.subjectchelerythrineen_US
dc.subjectnephrotoxicityen_US
dc.subjectprotein kinase Cen_US
dc.subjectreactive oxygen radicalsen_US
dc.subjectraten_US
dc.titleProtective effect of chelerythrine on gentamicin-induced nephrotoxicityen_US
dc.typeArticleen_US

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