Neuroprotective effects of 18 beta-glycyrrhetinic acid against bisphenol A-induced neurotoxicity in rats: involvement of neuronal apoptosis, endoplasmic reticulum stress and JAK1/STAT1 signaling pathway

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dc.authorid0000-0001-5608-554X
dc.contributor.authorÇağlayan, Cüneyt
dc.contributor.authorKandemir, Fatih Mehmet
dc.contributor.authorAyna, Adnan
dc.contributor.authorGür, Cihan
dc.contributor.authorKüçükler, Sefa
dc.contributor.authorDarendelioğlu, Ekrem
dc.date.accessioned2022-06-24T11:31:42Z
dc.date.available2022-06-24T11:31:42Z
dc.date.issued2022
dc.departmentTıp Fakültesi
dc.description.abstractThe exposure to bisphenol A (BPA) is inevitable owing to its common use in the production of polycarbonate plastics. Studies to reduce side effects are gaining importance since BPA causes severe toxicities in important tissues such as testes, lungs, brain, liver and kidney. The current study was planned to study ameliorative effect of 18 beta-glycyrrhetinic acid (18 beta-GA) on BPA induced neurotoxicity. Fourty Wistar albino rats were divided into five equal groups as follows: I-Control group, II-18 beta-GA group (100 mg/kg), III- BPA group (250 mg/kg), IV-250 mg/kg BPA +50 mg/kg 18 beta-GA group, V-250 mg/kg BPA +100 mg/kg 18 beta-GA group. BPA intoxication was associated with increased MDA level while reduced GSH concentration, activities of glutathione peroxidase, superoxide dismutase, and catalase. BPA supplementation caused apoptosis in the brain by up-regulating caspase-3 and Bax levels and down-regulating Bcl-2. BPA also caused endoplasmic reticulum (ER) stress by increasing mRNA transcript levels of PERK, IRE1, ATF-6 and GRP78. Additionally, it was observed that BPA administration activated JAK1/STAT1 signaling pathway and levels of TNF-alpha, NF-kappa B, p38 MAPK and INK in the brain. However, co-treatment with 18 beta-GA at a dose of 50 and 100 mg/kg considerably ameliorated oxidative stress, inflammation, apoptosis, ER stress and JAK1/STAT1 signaling pathway in brain tissue. Overall, the data of this study indicate that brain damage associated with BPA toxicity could be ameliorated by 18 beta-GA administration.
dc.identifier.doi10.1007/s11011-022-01027-z
dc.identifier.endpage-en_US
dc.identifier.issn0885-7490
dc.identifier.issn1573-7365
dc.identifier.issue-en_US
dc.identifier.pmid35699857
dc.identifier.scopusqualityQ2
dc.identifier.startpage-en_US
dc.identifier.urihttps:/dx.doi.org/10.1007/s11011-022-01027-z
dc.identifier.urihttps://hdl.handle.net/20.500.12451/9479
dc.identifier.volume-en_US
dc.identifier.wosWOS:000810865000001
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherSpringer
dc.relation.ispartofMetabolic Brain Disease
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/embargoedAccess
dc.subjectBisphenol A
dc.subject18?-glycyrrhetinic Acid
dc.subjectEndoplasmic Reticulum Stress
dc.subjectOxidative Stress
dc.subjectJAK1/STAT1 Signaling Pathway
dc.titleNeuroprotective effects of 18 beta-glycyrrhetinic acid against bisphenol A-induced neurotoxicity in rats: involvement of neuronal apoptosis, endoplasmic reticulum stress and JAK1/STAT1 signaling pathway
dc.typeArticle

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