Publication:
The neuroprotective effect of 1,25-dyhydroxyvitamin D 3 (calcitriol) and probiotics on the rotenone-induced neurotoxicity model in SH-SY5Y cells

dc.contributor.authorGül, Fatma Hazan
dc.contributor.authorBozkurt, Nuh Mehmet
dc.contributor.authorNoğay, Nalan Hakime
dc.contributor.authorÜnal, Gökhan
dc.contributor.buuauthorNOĞAY, NALAN HAKİME
dc.contributor.departmentSağlık Bilimleri Fakültesi
dc.contributor.departmentBeslenme ve Diyetetik Bölümü
dc.contributor.orcid0000-0002-9435-5755
dc.contributor.researcheridMBI-0869-2025
dc.date.accessioned2025-02-14T06:12:39Z
dc.date.available2025-02-14T06:12:39Z
dc.date.issued2024-11-21
dc.description.abstractThis study aimed to investigate the neuroprotective role of probiotics and 1,25-dyhydroxyvitamin D3 (calcitriol) against neurotoxicity on rotenone-induced human neuroblastoma cell line SH-SY5Y. Rotenone was administered to induce neurotoxic effects in SH-SY5Y cells. Calcitriol and probiotics were administered at different concentrations as pre- and post-treatment. The thiazolyl blue tetrazolium bromide (MTT) assay was performed to measure cell viability. Intracellular protein levels of antioxidant enzymes (protein tyrosine kinase (PTK), superoxide dismutase (SOD), glutathione peroxidase (GSH), glutathione reductase (GSR), and catalase (CAT)) were determined by the enzyme-linked immunosorbent assay (ELISA). Rotenone (150 nM) reduced (p < 0.001) cell viability compared to control cells. Single and combined pretreatments with probiotics (0.01 mg/ml, 0.05 mg/ml, and 0.1 mg/ml) and calcitriol (1.25 <mu>M, 2.5 mu M, and 5 mu M) increased (p < 0.05) cell viability compared to rotenone group. In the pre- and post-treatment design, all treatment groups increased the SOD and GSH levels and decreased the GSR levels compared to rotenone. None of the pretreatments reversed the PTK levels (except probiotics: 0.01 mg/ml). Calcitriol (2.5 <mu>M) increased the CAT levels in pretreatment design, and probiotics (0.05 mg/ml and 0.1 mg/ml) increased CAT levels in post-treatment design compared to rotenone group. Calcitriol and probiotics protect against rotenone-induced neurotoxicity in SH-SY5Y cells by decreasing reactive oxygen species (ROS) and increasing antioxidant enzyme parameters. These neuroprotective effects of calcitriol and probiotics against rotenone-induced dopaminergic neurotoxicity provide an experimental basis for their potential clinical use in the treatment of Parkinson's disease (PD).[GRAPHICS].
dc.identifier.doi10.1080/01480545.2024.2429621
dc.identifier.eissn1525-6014
dc.identifier.issn0148-0545
dc.identifier.scopus2-s2.0-85210168358
dc.identifier.urihttps://doi.org/10.1080/01480545.2024.2429621
dc.identifier.urihttps://www.tandfonline.com/doi/full/10.1080/01480545.2024.2429621
dc.identifier.urihttps://hdl.handle.net/11452/50383
dc.identifier.wos001363765600001
dc.indexed.wosWOS.SCI
dc.language.isoen
dc.publisherTaylor
dc.relation.journalDrug and Chemical Toxicology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectParkinsons-disease
dc.subjectVitamin-d
dc.subjectOxidative stress
dc.subjectNeurodegenerative diseases
dc.subjectExposure
dc.subjectPesticides
dc.subjectApoptosis
dc.subjectSurvival
dc.subjectGrowth
dc.subjectParkinson's disease
dc.subjectProbiotics
dc.subjectNeurotoxicity
dc.subjectNeuroprotective
dc.subjectSh-sy5y cell-line
dc.subject1,25-dyhydroxyvitamin d-3
dc.subjectScience & technology
dc.subjectPhysical sciences
dc.subjectLife sciences & biomedicine
dc.subjectChemistry, multidisciplinary
dc.subjectPharmacology & pharmacy
dc.subjectToxicology
dc.subjectChemistry
dc.titleThe neuroprotective effect of 1,25-dyhydroxyvitamin D 3 (calcitriol) and probiotics on the rotenone-induced neurotoxicity model in SH-SY5Y cells
dc.typeArticle
dc.typeEarly Access
dspace.entity.typePublication
local.contributor.departmentSağlık Bilimleri Fakültesi/Beslenme ve Diyetetik Bölümü
local.indexed.atWOS
local.indexed.atScopus
relation.isAuthorOfPublicationf4945ace-0c55-48af-bf5f-2015472ce72f
relation.isAuthorOfPublication.latestForDiscoveryf4945ace-0c55-48af-bf5f-2015472ce72f

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