Person: KOYUNCUOĞLU, TÜRKAN
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KOYUNCUOĞLU
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TÜRKAN
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Publication Metadata only Sıçanlarda parkinson hastalığına bağlı oluşan bellek disfonksiyonuna farklı egzersiz uygulamalarının etkileri(2022-05-12) KOYUNCUOĞLU, TÜRKAN; ÖZKAN YENAL, NAZİYE; KASIMAY ÇAKIR, ÖZGÜR; GÜLHAN, REZZAN; YÜKSEL, MERAL; Koyuncuoğlu T., Erol G., Çulpan Y., Gülhan R., Yüksel M., Özkan Yenal N., Kasımay Çakır Ö.Giriş: Parkinson hastalığı (PH) Alzheimer hastalığından sonra en yaygın görülennörodejeneratif hastalıktır.1 PH’da motor semptomların yanı sıra bellek disfonksiyonugörülmektedir. Yüksek anksiyete seviyeleri bellek fonksiyonlarını olumsuz etkilemektedir.2Amaç: İstemli tekerlek çevirme egzersizi, direnç egzersizi ve kombine egzersizuygulamalarının anksiyete düzeyleri ile bellek üzerindeki etkilerinin araştırılması ve alttayatan mekanizmaların ortaya konulması amaçlanmıştır.Yöntem: Çalışmada Wistar Albino erkek sıçanlarda (n=50) taklit cerrahi ve Parkinsongrupları oluşturulduktan sonra sedanter ve 3 farklı egzersiz protokolünün uygulandığı istemli(İE), rezistans (RE) ve kombine (KE: İE+RE) grupları oluşturuldu. Egzersizler 6 haftaboyunca (3 gün/hafta) uygulandı. PH modeli oluşturmak için sıçanlarda sağ mediyal önbeyine 6-OHDA (0.5 μl/dk) enjeksiyonu yapıldı. Taklit cerrahili gruplara 6-OHDA’nınçözücüsü verildi. Apomorfin uygulamaları sonrası rotasyon hareketi ile Parkinson modelideğerlendirildi. Obje tanıma testi ve delikli levha testleri sıçanlarda bellek fonksiyonlarını veanksiyete düzeylerini değerlendirmek için yaptırıldı. Beyin dokusunda antioksidan glutatyon(GSH) ve lipid peroksidasyonu belirteci malondialdehit (MDA) ve nötrofil infiltrasyonugöstergeci miyeloperoksidaz (MPO) aktivitesi, oksidan radikallerin belirteci luminol velusigenin ölçüldü. Verilerin analizinde tek yönlü ANOVA ardından Tukey-Kramer testi ilestudent’s t testi kullanıldı. Bulgular: Her 3 egzersiz ile Parkinsona bağlı gerileyen bellek fonksiyonu düzelmiştir(p<0.05-0.01). Sedantere kıyasla PH oluşturulmuş KE grubunda rotasyon hareketi azalırken,İE grubunda arttı (p<0.05-0.01). PH oluşturulmasıyla luminol ve lusigenin düzeyleri artarken,İE ile luminol azalmıştır (p<0.05-0.001). MPO aktivitesinin PH oluşturulmasıyla sedantergrubunda yükseldiği, ancak İE ve RE gruplarında baskılandığı gözlenmiştir (p<0.01-0.001).Her 3 egzersiz ile GSH düzeylerinin arttığı (p<0.05-0.01), KE ile MDA düzeylerinin düştüğübulundu (p<0.05). PH oluşturulmasıyla sedanter grupta azalmış bulunan bakılan delik sayısıve şahlanma sayısı (p<0.01-0.001), RE ve KE gruplarında artmıştır (p<0.05-0.01). Sedanterve İE gruplarında artan donma süresi, KE ile azalmıştır (p<0.05-0.001).Tartışma ve Sonuç: KE lipid peroksidasyonunu baskılamış, İE ve RE nötrofilinfiltrasyonunu azaltmıştır. RE ve KE anksiyeteyi hafifletmiştir. PH’da oluşan bellekdisfonksiyonunda farklı egzersiz uygulamalarının koruyucu etki gösterdikleri ortayakonmuştur.Anahtar Sözcükler: Egzersiz, Parkinson, Anksiyete, Bellek, AntioksidanPublication Metadata only Possible anti-inflammatory, antioxidant, and neuroprotective effects of apigenin in the setting of mild traumatic brain injury: an investigation*(2022-10-01) KOYUNCUOĞLU, TÜRKAN; YÜKSEL, MERAL; PEKER EYÜBOĞLU, İREM; AKAKIN, DİLEK; Kuru Bektasoglu P., Demir D., Koyuncuoglu T., YÜKSEL M., PEKER EYÜBOĞLU İ., Karagoz Koroglu A., AKAKIN D., Yildirim A., Celikoglu E., Gurer B.Objective Apigenin is a plant flavone proven with biological properties such as anti-inflammatory, antioxidant, and antimicrobial effects. This study, it was aimed to examine the possible anti-inflammatory, antioxidant, and neuroprotective effects of apigenin in the setting of the mild traumatic brain injury (TBI) model. Methods Wistar albino male rats were randomly assigned to groups: control (n = 9), TBI (n = 9), TBI + vehicle (n = 8), and TBI + apigenin (20 and 40 mg/kg, immediately after trauma; n = 6 and n = 7). TBI was performed by dropping a 300 g weight from a height of 1 m onto the skull under anesthesia. Neurological examination and tail suspension tests were applied before and 24 h after trauma, as well as Y-maze and object recognition tests, after that rats were decapitated. In brain tissue, luminol- and lucigenin-enhanced chemiluminescence levels and cytokine ELISA levels were measured. Histological damage was scored. Data were analyzed with one-way ANOVA. Results After TBI, luminol (p < .001) and lucigenin (p < .001) levels increased, and luminol and lucigenin levels decreased with apigenin treatments (p < .01-.001). The tail suspension test score increased with trauma (p < .01). According to the pre-traumatic values, the number of entrances to the arms (p < .01) in the Y-maze decreased after trauma (p < .01). In the object recognition test, discrimination (p < .05) and recognition indexes (p < .05) decreased with trauma. There was no significant difference among trauma apigenin groups in behavioral tests. Interleukin (IL)-10 levels, one of the anti-inflammatory cytokines, decreased with trauma (p < .05), and increased with 20 and 40 mg apigenin treatment (p < .001 and p < .01, respectively). The histological damage score in the cortex was decreased in the apigenin 20 mg treatment group significantly (p < .05), but the decrease observed in the apigenin 40 mg group was not significant. Conclusion The results of this study revealed that apigenin 20 and 40 mg treatment may have neuroprotective effects in mild TBI via decreasing the level of luminol and lucigenin and increasing the IL-10 levels. Additionally, apigenin 20 mg treatment ameliorated the trauma-induced cortical tissue damage.Publication Open Access Anti-inflammatory, antioxidant and neuroprotective effects of niacin on mild traumatic brain injury in rats(2023-01-01) KOYUNCUOĞLU, TÜRKAN; AKAKIN, DİLEK; ERZİK, CAN; YÜKSEL, MERAL; YEGEN, BERRAK; Ozaydin D., Bektasoglu P. K., Koyuncuoglu T., Ozkaya S. C., Koroglu A. K., AKAKIN D., ERZİK C., YÜKSEL M., YEGEN B., Gurer B.AIM: To study the effects of niacin, a water-soluble vitamin, on inflammation, oxidative stress and apoptotic processes observed after mild traumatic brain injury (TBI). MATERIAL and METHODS: A total of 25 Wistar albino male rats were randomly divided into control (n=9), TBI + Placebo group (n=9), TBI + niacin (500 mg/kg; n=7) groups. Mild TBI was performed under anesthesia by dropping a 300 g weight from a height of 1 meter onto the skull. Behavioral tests were applied before and 24 hours after TBI. Luminol and lucigenin levels and tissue cytokine levels were measured. Histopathological damage was scored in brain tissue. RESULTS: After mild TBI, luminol and lucigenin levels were increased (p<0.001), and their levels were decreased with niacin treatment (p<0.01-p<0.001). An increased score was obtained with trauma in the tail suspension test (p<0.01), showing depressive behavior. The number of entries to arms in Y-maze test were decreased in TBI group compared to pre-traumatic values (p<0.01), while discrimination (p<0.05) and recognition indices (p<0.05) in object recognition test were decreased with trauma, but niacin treatment did not change the outcomes in behavioral tests. Levels of the anti-inflammatory cytokine IL-10 were decreased with trauma, and increased with niacin treatment (p<0.05). The histological damage score was increased with trauma (p<0.001), and decreased with niacin treatment in the cortex (p<0.05), and hippocampal dentate gyrus region (p<0.01). CONCLUSION: Niacin treatment after mild TBI inhibited trauma-induced production of reactive oxygen derivatives and elevated the anti-inflammatory IL-10 level. Niacin treatment ameliorated the histopathologically evident damage.Publication Open Access Nesfatin-1 ameliorates oxidative brain damage and memory impairment in rats induced with a single acute epileptic seizure(2022-04-01) ARABACI TAMER, SEVİL; KOYUNCUOĞLU, TÜRKAN; AKAKIN, DİLEK; YÜKSEL, MERAL; YEGEN, BERRAK; Arabacı Tamer S., Koyuncuoğlu T., Karagöz Köroğlu A., AKAKIN D., YÜKSEL M., YEGEN B.© 2022Aims: We aimed to investigate putative neuroprotective effects of nesfatin-1 on oxidative brain injury and memory dysfunction induced by a single epileptic seizure and to compare these effects with those of antiepileptic phenytoin. Main methods: Wistar albino rats were randomly divided into a control group and pentylenetetrazole (PTZ)-seizure groups pretreated intraperitoneally (ip) with saline or nesfatin-1 (NES-1; 0.3, 1 or 3 μg/kg/day) or phenytoin (PHE; 40 mg/kg/day) or PHE + NES-1 (0.3 μg/kg/day) at 30 min before the single-dose PTZ injection (45 mg/kg; ip). All treatments were repeated at the 24th and 48th h of the provoked epileptic seizure. Passive-avoidance test was performed to assess memory function. The rats were decapitated at the 72nd hour of seizures and brain tissues were analyzed for histopathological changes and for measuring levels of malondialdehyde, glutathione, myeloperoxidase activity and reactive oxygen/nitrogen species. Key findings: In parallel to the effects of phenytoin, NES-1 reduced seizure score, elevated antioxidant glutathione content, depressed generation of nitric oxide and protected against seizure-induced neuronal damage. Additionally, increased malondialdehyde levels and elevated glial fibrillary acidic protein immunoreactivity in the cortex and hippocampus were decreased and memory dysfunction was improved by NES-1. However, NES-1 had no impact on myeloperoxidase activity or production of reactive oxygen species in the brain. Significance: The findings of the present study demonstrate that nesfatin-1 treatment provides neuroprotection against seizure-induced oxidative damage and memory dysfunction by inhibiting reactive nitrogen species and upregulating antioxidant capacity, indicating its potential in alleviating memory deficits and increasing the effectiveness of conventional anti-convulsant therapies.