Ex vivo investigation of betaine and boric acid function as preprotective agents on rat synaptosomes to be treated with A? (1-42)

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dc.authoridÇakır Gündoğdu, Ayşe/0000-0002-2466-9417en_US
dc.authoridOzbayer, Cansu/0000-0002-1120-1874en_US
dc.authoridHacioglu, Ceyhan/0000-0002-0993-6118en_US
dc.authorscopusid57208671422en_US
dc.authorscopusid57208669078en_US
dc.authorscopusid36195006500en_US
dc.authorscopusid59193870300en_US
dc.authorwosidÇakır Gündoğdu, Ayşe/ABE-4977-2020en_US
dc.authorwosidOzbayer, Cansu/F-6442-2015en_US
dc.contributor.authorHacioglu, Ceyhan
dc.contributor.authorKar, Fatih
dc.contributor.authorOzbayer, Cansu
dc.contributor.authorGundogdu, Ayse Cakir
dc.date.accessioned2024-08-23T16:07:17Z
dc.date.available2024-08-23T16:07:17Z
dc.date.issued2024en_US
dc.departmentDüzce Üniversitesien_US
dc.description.abstractRecent evidence suggests that ferroptosis, an iron-dependent cell death process, may be involved in Alzheimer's disease (AD) pathology. The study evaluated the therapeutic potential of betaine and boric acid (BA) pretreatment administered to rats for 21 days in AD. Then, the rats were sacrificed, and morphological and biochemical analyses were performed in brain tissues. Next, an ex vivo AD model was created by applying amyloid-beta (A beta 1-42) to synaptosomes isolated from the brain tissues. Synaptosomes were analyzed with micrograph images, and protein and mRNA levels of ferroptotic markers were determined. Betaine and BA pretreatments did not cause any morphological and biochemical differences in the brain tissue. However, A beta (1-42) administration in synaptosomes increased the levels of acyl-CoA synthetase long chain family member-4 (ACSL4), transferrin receptor-1 protein (TfR1), malondialdehyde (MDA), and 8-hydroxydeoxyguanosine (8-OHdG) and decreased the levels glutathione peroxidase-4 (GPx4) and glutathione (GSH). Moreover, ACSL4, GPx4, and TfR1 mRNA and protein levels were similar to the ELISA results. In contrast, betaine and BA pretreatments decreased the levels of ACSL4, TfR1, MDA, and 8-OHdG in synaptosomes incubated with A beta 1-42, while promoting increased levels of GPx4 and GSH. In addition, betaine and BA pretreatments completely reversed ACSL4, GPx4, and TfR1 mRNA and protein levels. Therefore, betaine and BA pretreatments may contribute to the prevention of neurodegenerative damage by supporting antiferroptotic activities.en_US
dc.description.sponsorshipTuerkiye Bilimsel ve Teknolojik Arastimath;rma Kurumuen_US
dc.description.sponsorshipTuerkiye Bilimsel ve Teknolojik Arast & imath;rma Kurumuen_US
dc.identifier.doi10.1002/tox.24098
dc.identifier.endpage2149en_US
dc.identifier.issn1520-4081
dc.identifier.issn1522-7278
dc.identifier.issue4en_US
dc.identifier.pmid38108610en_US
dc.identifier.scopus2-s2.0-85179908918en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage2138en_US
dc.identifier.urihttps://doi.org/10.1002/tox.24098
dc.identifier.urihttps://hdl.handle.net/20.500.12684/14566
dc.identifier.volume39en_US
dc.identifier.wosWOS:001126711000001en_US
dc.identifier.wosqualityQ1en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherWileyen_US
dc.relation.ispartofEnvironmental Toxicologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectAlzheimer's diseaseen_US
dc.subjectbetaineen_US
dc.subjectboric aciden_US
dc.subjectferroptosisen_US
dc.subjectiron metabolismen_US
dc.subjectTfRen_US
dc.subjectGlutathione-Peroxidase 4en_US
dc.subjectAlzheimers-Diseaseen_US
dc.subjectIronen_US
dc.subjectTransferrinen_US
dc.subjectBrainen_US
dc.titleEx vivo investigation of betaine and boric acid function as preprotective agents on rat synaptosomes to be treated with A? (1-42)en_US
dc.typeArticleen_US

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