Neuroprotective Effects of Eexenatide in a Rotenone-Induced Rat Model of Parkinson's Disease

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dc.authoridÇavuşoğlu, Türker/0000-0001-7100-7080
dc.authoridAksoy, Dürdane/0000-0003-1981-084X
dc.authoridates, utku/0000-0002-7709-3626
dc.authoridsolmaz, volkan/0000-0002-9045-2347
dc.authoridMeral, Ayfer/0000-0002-8870-3725
dc.authoridErbas, Oytun/0000-0001-5427-8428
dc.authorwosidMeral, Ayfer/HJB-0547-2022
dc.authorwosidÇavuşoğlu, Türker/AAJ-9609-2020
dc.authorwosidAksoy, Dürdane/B-7835-2017
dc.authorwosidERBAS, OYTUN/ABA-7380-2021
dc.authorwosidates, utku/J-1542-2015
dc.authorwosidATEŞ, UFUK/HGA-3970-2022
dc.contributor.authorAksoy, Durdane
dc.contributor.authorSolmaz, Volkan
dc.contributor.authorCavusoglu, Turker
dc.contributor.authorMeral, Ayfer
dc.contributor.authorAtes, Utku
dc.contributor.authorErbas, Oytun
dc.date.accessioned2024-06-12T11:12:05Z
dc.date.available2024-06-12T11:12:05Z
dc.date.issued2017
dc.departmentTrakya Üniversitesien_US
dc.description.abstractBackround: Several studies suggest an association between Parkinson's disease (PD) and type 2 diabetes mellitus; these 2 diseases are both known to affect the common molecular pathways. As a synthetic agonist for the glucagon-like peptide 1 receptor, exenatide has been evaluated as a neuroprotective agent in multiple animal models. Rotenone models of PD have great potential for the investigation of PD pathology and motor and nonmotor symptoms, as well as the role of gene environment interactions in PD causation and pathogenesis. Therefore, in this study, the neurochemical, behavioral and histologic effects of exenatide on a rotenone-induced rat model of PD were examined. Materials and Methods: Eighteen adult male rats were randomly divided into the following 3 groups (n = 6): 1 group received stereotaxical infusion of dimethyl sulfoxide (vehicle, group 1) and the others received stereotaxical infusion of rotenone (groups 2 and 3). Apomorphine-induced rotation test was applied to the rats after 10 days. Thereafter, group 2 was administered isotonic saline, whereas group 3 was administered exenatide for 28 days. Results: Malondialdehyde and tumor necrosis factor alpha levels increased in the rats with PD induced by rotenone, whereas malondialdehyde and tumor necrosis factor alpha levels markedly decreased in the rats treated with exenatide. The apomorphine-induced rotation test scores of exenatide-treated rats were determined to be lower compared with the untreated group. Additionally, treatment with exenatide significantly reduced the loss of dopaminergic neurons in striatum. Conclusions: These results have shown that exenatide has neuroprotective, anti-inflammatory and antioxidant effects in a rotenone-induced rat model of PD.en_US
dc.identifier.endpage324en_US
dc.identifier.issn0002-9629
dc.identifier.issn1538-2990
dc.identifier.issue3en_US
dc.identifier.pmid28918840en_US
dc.identifier.scopus2-s2.0-85030439965en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage319en_US
dc.identifier.urihttps://hdl.handle.net/20.500.14551/23042
dc.identifier.volume354en_US
dc.identifier.wosWOS:000410832600017en_US
dc.identifier.wosqualityQ2en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherElsevier Science Incen_US
dc.relation.ispartofAmerican Journal Of The Medical Sciencesen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectParkinson's Diseaseen_US
dc.subjectRotenoneen_US
dc.subjectGlucagon-Like Peptide 1en_US
dc.subjectExenatideen_US
dc.subjectTumor Necrosis Factor Alphaen_US
dc.subjectGlucagon-Like Peptide-1en_US
dc.subjectDopaminergic-Neuronsen_US
dc.subjectOxidative Stressen_US
dc.subjectAnimal-Modelen_US
dc.subjectReceptoren_US
dc.subjectBrainen_US
dc.subjectMechanismsen_US
dc.subjectExenatideen_US
dc.subjectSystemen_US
dc.subjectNeuroinflammationen_US
dc.titleNeuroprotective Effects of Eexenatide in a Rotenone-Induced Rat Model of Parkinson's Diseaseen_US
dc.typeArticleen_US

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