Effect of Epigallocatechin Gallate on Cisplatin-Induced Nephrotoxicity in Rats

dc.contributor.authorTimurkaan, Mustafa
dc.contributor.authorDemir, Mustafa
dc.contributor.authorGomleksiz, Muhammet Ridvan
dc.contributor.authorOzercan, Ibrahim Halil
dc.contributor.authorŞahin, Kazım
dc.contributor.authorDogukan, Ayhan
dc.date.accessioned2026-08-12T17:06:50Z
dc.date.issued2021
dc.departmentFırat Üniversitesi
dc.description.abstractObjectives: Nephrotoxicity caused by CDDP is attributed to an increase in kidney oxidative stress, which restricts the therapeutic application of CDDP. EGCG is a very strong green tea-derived antioxidant. To investigate the effect of epigallocatechin gallate (EGCG) on cisplatin (CDDP)-induced lipid peroxidation and nephrotoxicity in rats. Methods: Twenty-eight male Wistar rats (8 weeks, 200-215 g) were used in the research and were separated into 4 equal groups: (1) control rats, (2) EGCG (100 mg/kg, daily) control rats, (3) CDDP-injected rats, CDDP group (7 mg/kg, i.p., single dose), and (4) EGCG-treated (100 mg/kg, daily) plus CDDP-injected rats (EGCG + CDDP group). Results: There was a substantial rise in malondialdehyde (MDA) levels in the CDDP-injected rats (P <.05). The EGCG prevented the rise of the MDA (P <.05). In CDDP-injected rats, renal Bax protein expression was substantially higher compared with control rats, and EGCG therapy significantly decreased Bax protein levels (P <.05). In EGCG + CDDPadministered rats, Bcl-2 protein expression was higher than in CDDP-injected rats (P <.05). In the EGCG + CDDP group, the expression of renal heat shock protein 60 (Hsp60) and heat shock protein 70 (HSP70) was significantly lower compared to CDDP-alone injected rats (P <.001). CDDP-induced renal histopathological changes were significantly improved with EGCG. Conclusion: CDDP produces oxidative stress and renal damage. The EGCG that reduces oxidative stress and changes the expression of Bax and Bcl-2 proteins may potentially have a signi.cant role in the prevention of CDDP-induced renal injury.
dc.description.sponsorshipFirat University Scientific Research Center
dc.description.sponsorshipThe authors declared that this study has received financial support from Firat University Scientific Research Center.
dc.identifier.doi10.5152/turkjnephrol.2021.21027
dc.identifier.endpage268
dc.identifier.issn2667-4440
dc.identifier.issue4
dc.identifier.orcid0000-0001-9542-5244
dc.identifier.scopus2-s2.0-85128669462
dc.identifier.scopusqualityQ4
dc.identifier.startpage262
dc.identifier.trdizinid478990
dc.identifier.urihttps://doi.org/10.5152/turkjnephrol.2021.21027
dc.identifier.urihttps://search.trdizin.gov.tr/tr/yayin/detay/478990
dc.identifier.urihttps://hdl.handle.net/11508/49421
dc.identifier.volume30
dc.identifier.wosWOS:000710457200003
dc.identifier.wosqualityQ4
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakTR-Dizin
dc.language.isoen
dc.publisherAves
dc.relation.ispartofTurkish Journal of Nephrology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.snmzKA_WoS_20260511
dc.subjectCisplatin
dc.subjectnephrotoxicity
dc.subjectepigallocatechin gallate
dc.subjectmalondialdehyde
dc.subjectBax/bcl-2
dc.subjectHsp60-70
dc.titleEffect of Epigallocatechin Gallate on Cisplatin-Induced Nephrotoxicity in Rats
dc.typeArticle

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