Please use this identifier to cite or link to this item: https://hdl.handle.net/11499/58707
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dc.contributor.authorDarendelioglu, Ekrem-
dc.contributor.authorCaglayan, Cuneyt-
dc.contributor.authorKucukler, Sefa-
dc.contributor.authorBayav, Brahim-
dc.contributor.authorKandemir, Fatih Mehmet-
dc.contributor.authorAyna, Adnan-
dc.contributor.authorSag, Sevda-
dc.date.accessioned2025-01-22T17:15:43Z-
dc.date.available2025-01-22T17:15:43Z-
dc.date.issued2025-
dc.identifier.issn0278-6915-
dc.identifier.issn1873-6351-
dc.identifier.urihttps://doi.org/10.1016/j.fct.2024.115218-
dc.description.abstractBisphenol A (BPA) has been commonly used in various consumer products, including water bottles, food containers, and canned food linings. However, there are concerns about its potential toxicity to human health, particularly its impact on the liver and kidneys. The objective of this research was to investigate the potential ameliorative effects of 18(3-glycyrrhetinic acid (GA) against BPA-induced hepatotoxicity and nephrotoxicity in rats. The animals were supplemented with BPA (250 mg/kg b.w.) alone or with GA (50 and 100 mg/kg b.w.) for 14 days. GA treatment alleviated the BPA-induced hepato-renal tissue injuries through reducing the serum ALT, AST and ALP levels, and urea and creatinine levels. GA co-treatment also increased activities of SOD, CAT and GPx enzymes and levels of GSH, and suppressed MDA levels in BPA induced tissues. BPA also induced inflammation by increasing the levels of TNF-alpha, NF-kappa B, JAK1, STAT1, P38 MAPK and JNK in liver and kidney tissues and GA treatment ameliorated these effects. BPA triggered apoptosis by increasing caspase-3, Bax, and cytochrome c at protein levels and also by decreasing the antiapoptotic Bcl-2 level. However, treatment with GA (50 and 100 mg/kg) decreased apoptosis. Overall, our results have revealed the potential ameliorative mechanisms of GA, as a possible agent for BPA-induced hepatotoxicity and nephrotoxicity.en_US
dc.description.sponsorshipScientific Research Projects Coordination Unit of Bingol University [BAP-FEF.2020.00.006]en_US
dc.description.sponsorshipThis work was supported by Grants from the Scientific Research Projects Coordination Unit of Bingol University (Project Code: BAP-FEF.2020.00.006). Therefore, we are grateful to Bingol University, Turkey.en_US
dc.language.isoenen_US
dc.publisherPergamon-elsevier Science Ltden_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectApoptosisen_US
dc.subjectBisphenol Aen_US
dc.subjectHepatotoxicityen_US
dc.subjectInflammationen_US
dc.subjectNephrotoxicityen_US
dc.subject18(3-Glycyrrhetinic Aciden_US
dc.title18(3-Glycyrrhetinic Acid Mitigates Bisphenol A-Induced Liver and Renal Damage: Inhibition of Tnf-α/Nf-κb Jak1/Stat1 Pathways, Oxidative Stress and Apoptosisen_US
dc.typeArticleen_US
dc.identifier.volume196en_US
dc.departmentPamukkale Universityen_US
dc.identifier.doi10.1016/j.fct.2024.115218-
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.authorwosidDARENDELİOĞLU, Ekrem/ABI-5581-2020-
dc.authorwosidAyna, Adnan/AAE-6567-2021-
dc.identifier.pmid39722417-
dc.identifier.scopus2-s2.0-85212952678-
dc.identifier.wosWOS:001400181100001-
dc.identifier.scopusqualityQ1-
dc.description.woscitationindexScience Citation Index Expanded-
dc.identifier.wosqualityQ1-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.grantfulltextnone-
item.fulltextNo Fulltext-
item.languageiso639-1en-
item.cerifentitytypePublications-
item.openairetypeArticle-
Appears in Collections:PubMed İndeksli Yayınlar Koleksiyonu / PubMed Indexed Publications Collection
Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection
Tıp Fakültesi Koleksiyonu
WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection
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