Amelioration of rotenone-induced dopaminergic cell death in the striatum by oxytocin treatment

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dc.contributor.authorErbas, Oytun
dc.contributor.authorOltulu, Fatih
dc.contributor.authorTaskiran, Dilek
dc.date.accessioned2019-10-27T21:40:46Z
dc.date.available2019-10-27T21:40:46Z
dc.date.issued2012
dc.departmentEge Üniversitesien_US
dc.description.abstractOxytocin (OT) is essentially associated with uterine contraction during parturition and milk ejection reflex. Although several studies implicate the role of OT in anti-inflammatory, anti-oxidative and anti-apoptotic pathways, there is a lack of data with regard to the protective effects of oxytocin in neurodegenerative models such as Parkinson's disease (PD). The present study was undertaken to investigate the neuroprotective effects of oxytocin (OT) on rotenone-induced PD in rats. Twenty adult Sprague-Dawley rats were injected with rotenone (3 mu g/mu l in DMSO) or vehicle (1 mu l DMSO) into the left substantia nigra pars compacta (SNc) and ventral tegmental area (VTA) under stereotaxic surgery, and PD model was assessed by rotational test ten days after drug infusion. The valid PD rats were randomly divided into two groups; Group 1 (n = 7) and Group 2 (n = 7) were administered saline (1 ml/kg/day, i.p.) and oxytocin (160 mu g/kg/day, i.p.) through 20 days, respectively. The effects of OT treatment were evaluated by behavioral, histological and immunohistochemical parameters. Apomorphine-induced stereotypic rotations in PD rats were significantly inhibited by OT treatment (p < 0.05). In addition, immunohistochemical studies clearly demonstrated the suppression of Bax, caspase-3, caspase-8 and elevation of Bcl-2 and tyrosine hydroxylase immunoexpression in OT-treated rats compared to saline group. Our findings suggest that oxytocin may have cytoprotective and restorative effects on dopaminergic neurons against rotenone-induced injury. The underlying mechanism may be associated with the inhibition of apoptotic pathways. (C) 2012 Elsevier Inc. All rights reserved.en_US
dc.identifier.doi10.1016/j.peptides.2012.05.026en_US
dc.identifier.endpage317en_US
dc.identifier.issn0196-9781
dc.identifier.issn1873-5169
dc.identifier.issue2en_US
dc.identifier.pmid22985856en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage312en_US
dc.identifier.urihttps://doi.org/10.1016/j.peptides.2012.05.026
dc.identifier.urihttps://hdl.handle.net/11454/46355
dc.identifier.volume38en_US
dc.identifier.wosWOS:000313610600013en_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.ispartofPeptidesen_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.subjectOxytocinen_US
dc.subjectNeuroprotectionen_US
dc.subjectAnimal modelsen_US
dc.titleAmelioration of rotenone-induced dopaminergic cell death in the striatum by oxytocin treatmenten_US
dc.typeArticleen_US

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