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dc.contributor.authorErbas, Oytun
dc.contributor.authorTaskiran, Dilek
dc.contributor.authorOltulu, Fatih
dc.contributor.authorYavasoglu, Altug
dc.contributor.authorBora, Saylav
dc.contributor.authorBilge, Okan
dc.contributor.authorPeker, Gonul
dc.date.accessioned2019-08-13T12:10:23Z
dc.date.accessioned2019-08-13T15:56:36Z
dc.date.available2019-08-13T12:10:23Z
dc.date.available2019-08-13T15:56:36Z
dc.date.issued2017
dc.identifier.issn0161-6412
dc.identifier.issn1743-1328
dc.identifier.urihttps://dx.doi.org/10.1080/01616412.2016.1249630
dc.identifier.urihttp://hdl.handle.net/11446/2341
dc.descriptionWOS: 000390431000008en_US
dc.descriptionPubMed ID: 27881053en_US
dc.description.abstractPurpose: The aim of the present study is to investigate the protective effects of oxytocin (OT) on diabetic neuropathy (DNP) in rats. Materials and methods: Eighteen rats were used to induce diabetes using single dose streptozotocin (STZ, 60 mg/kg). Diabetic DNP was verified by electromyography (EMG) and motor function test on 21st day following STZ injection. Six rats served as naive control group and received no drug (n=6). Following EMG, diabetic rats were randomly divided into three groups and administered with either 1ml/kg saline or 80 g/kg OT or 160 g/kg OT intraperitoneally for four weeks. Then, EMG, motor function test, biochemical analysis (plasma lipid peroxides and glutathione), histological, and immunohistochemical analysis of sciatic nerves (bax, caspase 3, caspase 9, and NGF) were performed. Results: Diabetic rats developed neuropathy, which was apparent from decreased compound muscle action potentials amplitudes and prolonged distal latency in saline-treated rats (p<0.001) whereas 160 g/kg OT significantly improved EMG findings. OT treatment significantly lessened the thickening of perineural fibrosis when compared with saline group (p<0.001). Besides, OT significantly reduced plasma lipid peroxides (p<0.05) and increased glutathione levels in diabetic rats (p<0.001). The sciatic nerves of saline-treated rats showed considerable increase in bax, caspase 3 and caspase 8 expressions (p<0.001) while OT treatment significantly suppressed these apoptosis markers. Also, OT improved NGF expression in diabetic rats compared to saline group. Conclusion: Present results demonstrate that OT appears to alleviate harmful effects of hyperglycemia on peripheral neurons by suppressing inflammation, oxidative stress and apoptotic pathways.en_US
dc.description.sponsorshipEge University Research Fund [2010-TIP-066]en_US
dc.description.sponsorshipThis study was supported by the Ege University Research Fund (2010-TIP-066).en_US
dc.language.isoengen_US
dc.publisherTAYLOR & FRANCIS LTDen_US
dc.identifier.doi10.1080/01616412.2016.1249630en_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectDiabetes mellitusen_US
dc.subjectDiabetic polyneuropathyen_US
dc.subjectOxytocinen_US
dc.subjectEMGen_US
dc.subjectOxidative stressen_US
dc.titleOxytocin provides protection against diabetic polyneuropathy in ratsen_US
dc.typearticleen_US
dc.relation.journalNEUROLOGICAL RESEARCHen_US
dc.departmentDBÜen_US
dc.identifier.issue1en_US
dc.identifier.volume39en_US
dc.identifier.startpage45en_US
dc.identifier.endpage53en_US
dc.contributor.authorID0000-0002-4505-0939en_US
dc.contributor.authorID0000-0002-8993-2271en_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.department-temp[Erbas, Oytun] Istanbul Bilim Univ, Sch Med, Dept Physiol, Istanbul, Turkey -- [Taskiran, Dilek -- Bora, Saylav -- Peker, Gonul] Ege Univ, Sch Med, Dept Physiol, Izmir, Turkey -- [Oltulu, Fatih -- Yavasoglu, Altug] Ege Univ, Sch Med, Dept Histol & Embryol, Izmir, Turkey -- [Bilge, Okan] Ege Univ, Sch Med, Dept Anat, Izmir, Turkey -- [Cinar, Bilge Piri] Giresun State Hosp, Dept Neurol, Giresun, Turkeyen_US


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