Person: KOYUNCUOĞLU, TÜRKAN
Loading...
Email Address
Birth Date
Research Projects
Organizational Units
Job Title
Last Name
KOYUNCUOĞLU
First Name
TÜRKAN
Name
5 results
Search Results
Now showing 1 - 5 of 5
Publication 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 Metadata only Neuroprotective Effect of Plasminogen Activator Inhibitor-1 Antagonist in the Rat Model of Mild Traumatic Brain Injury(SPRINGER/PLENUM PUBLISHERS, 2021) ERZİK, CAN; Kuru Bektasoglu, Pinar; Koyuncuoglu, Turkan; Akbulut, Selin; Akakin, Dilek; Eyuboglu, Irem Peker; Erzik, Can; Yuksel, Meral; Kurtel, HizirPlasminogen activator inhibitor-1 (PAI-1) antagonists are known for their neuroprotective effects. In this study, it was aimed to investigate the possible protective effects of PAI-1 antagonists in a rat mild traumatic brain injury (TBI) model. Sprague-Dawley male rats were grouped as sham (n = 7), TBI (n = 9), and TBI + PAI-1 antagonist (5 and 10 mg/kg TM5441 and TM5484; n = 6-7). Under anesthesia, TBI was induced by dropping a metal 300-g weight from a height of 1 m on the skull. Before and 24-h after trauma neurological examination, tail suspension, Y-maze, and novel object recognition tests were performed. Twenty-four hours after TBI, the rats were decapitated and activities of myeloperoxidase, nitric oxide release, luminol-, and lucigenin-enhanced chemiluminescence were measured. Also, interleukin-1 beta, interleukin-6, tumor necrosis factor, interleukin-10, tumor growth factor-beta, caspase-3, cleaved caspase-3, and PAI levels were measured with the ELISA method in the brain tissue. Brain injury was graded histopathologically following hematoxylin-eosin staining. Western blot and immunohistochemical investigation for low-density lipoprotein receptor, matrix metalloproteinase-3, and nuclear factor-kappa B were also performed. Data were analyzed using GraphPad Prism 8.0 (GraphPad Software, San Diego, CA, USA) and expressed as means +/- SEM. Values of p < 0.05 were considered to be statistically significant. Higher levels of myeloperoxidase activity in the TBI group (p < 0.05) were found to be suppressed in 5 and 10 mg/kg TM5441 treatment groups (p < 0.05-p < 0.01). The tail suspension test score was increased in the TBI group (p < 0.001) and decreased in all treatment groups (p < 0.05-0.001). The histologic damage score was increased statistically significantly in the cortex, dentate gyrus, and CA3 regions in the TBI group (p < 0.01-0.001), decreased in the treatment groups in the cortex and dentate gyrus (p < 0.05-0.001). PAI antagonists, especially TM5441, have antioxidant and anti-inflammatory properties against mild TBI in the acute period. Behavioral test results were also improved after PAI antagonist treatment after mild TBI.Publication Metadata only Neuroprotective Effect of Cinnamaldehyde on Secondary Brain Injury After Traumatic Brain Injury in a Rat Model(ELSEVIER SCIENCE INC, 2021) YEGEN, BERRAK; Bektasoglu, Pinar Kuru; Koyuncuoglu, Turkan; Demir, Dilan; Sucu, Gizem; Akakin, Dilek; Eyuboglu, Irem Peker; Yuksel, Meral; Celikoglu, Erhan; Yegen, Berrak C.; Gurer, BoraOBJECTIVE: The aim of this study was to investigate the possible neuroprotective effects of cinnamaldehyde (CA) on secondary brain injury after traumatic brain injury (TBI) in a rat model. METHODS: Rats were randomly divided into 4 groups: control (n = 9), TBI (n = 9), vehicle (0.1% Tween 80; n = 8), and CA (100 mg/kg) (n = 9). TBI was induced by the weight-drop model. In brain tissues, myeloperoxidase ac-tivity and the levels of luminol-enhanced and lucigenin-enhanced chemiluminescence were measured. Inter-leukin 1b, interleukin 6, tumor necrosis factor a, tumor growth factor b, caspase-3, and cleaved caspase-3 were evaluated with an enzyme-linked immunosorbent assay method. Brain injury was histopathologically graded after hematoxylin-eosin staining. Y-maze and novel object recognition tests were performed before TBI and within 24 hours of TBI. RESULTS: Higher myeloperoxidase activity levels in the TBI group (P < 0.001) were suppressed in the CA group (P < 0.05). Luminol-enhanced and lucigenin-enhanced chem-iluminescence, which were increased in the TBI group (P < 0.001, for both), were decreased in the group that received CA treatment (P < 0.001 for both). Compared with the increased histologic damage scores in the cerebral cortex and dentate gyrus of the TBI group (P < 0.001), scores of the CA group were lower (P < 0.001). Decreased number of entries and spontaneous alternation percentage in the Y-maze test of the TBI group (P < 0.05 and P < 0.01, respec-tively) were not evident in the CA group. CONCLUSIONS: CA has shown neuroprotective effects by limiting neutrophil recruitment, suppressing reactive oxygen species and reducing histologic damage and acute hippocampal dysfunction.Publication Metadata only Obestatin improves oxidative brain damage and memory dysfunction in rats induced with an epileptic seizure(ELSEVIER SCIENCE INC, 2017) YEGEN, BERRAK; Koyuncuoglu, Turkan; Vizdiklar, Caner; Uren, Dogan; Yilmaz, Hakan; Yildirim, Cagan; Atal, Sefa Semih; Akakin, Dilek; Demirci, Elif Kervancioglu; Yuksel, Meral; Yegen, Berrak C.Obestatin was shown to alleviate renal, gastrointestinal and haemorrhage-induced brain injury in rats. In order to investigate the neuroprotective effects of obestatin on seizure-induced oxidative brain injury, an epileptic seizure was induced with a single intraperitoneal (i.p.) close of pentylenetetrazole (PTZ, 45 mg/kg) in male Wistar rats. Thirty minutes before the PTZ injection, rats were treated with either saline or obestatin (1 mu g/kg, i.p.). Seizure was video-taped and then evaluated by using Racine's scoring (0-5). For the assessment of memory function, passive-avoidance test was performed before seizure induction, which was repeated on the 3rd day of seizure. The rats were decapitated at the 24th or 72nd hour of seizures and brain tissues were obtained for histopathological examination and for measuring levels of malondialdehyde (MDA), glutathione (GSH), reactive oxygen radicals and myeloperoxidase (MPO) activity. Obestatin treatment reduced the average seizure score, decreased the occurrence and duration of generalized tonic-clonic seizures, presenting with a shorter latency to their onset. Increased lipid peroxidation and enhanced generation of oxygen-derived radicals detected at the post-seizure 72nd h were suppressed by the consecutive treatments of obestatin, but no changes were observed by the single obestatin treatment in the 24-h seizure group. Neuronal damage and increased GFAP immunoreactivity, observed in the hippocampal areas and cortex of PTZ-induced rats were alleviated in 3-day obestatin-treated PTZ group. PTZ-induced memory dysfunction was significantly improved in obestatin-treated PTZ group as compared to saline-treated rats. The present data indicate that obestatin ameliorated the severity of PTZ-induced seizures, improved memory dysfunction and reduced neuronal damage by limiting oxidative damage. (C) 2017 Elsevier Inc. All rights reserved.Publication Open Access Nicorandil preserves blood-brain barrier and improves memory impairment in hypertensive rats(MARMARA UNIV, 2019-11-15) YEGEN, BERRAK; Cevikelli Yakut, Zatiye Ayca; Ertas, Busra; Koyuncuoglu, Turkan; Yegen, Berrak C.; Sener, GokselIn renovascular hypertension (RVH), oxidative stress and inflammation due to high blood pressure and elevated levels of angiotensin 2 are mainly responsible of cerebrovascular complications and impaired cognitive functions. Since the nicorandil has been shown to exert neuroprotective, anti-inflammatory and antioxidant effects, we investigated the effect of nicorandil against vascular dementia and blood brain barrier damage in a rat model of angiotensin-dependent hypertension. Wistar albino rats, were divided as sham-operated control, renovascular hypertension (RVH) and Nicorandil-treated RVH groups. Silver clip was implanted onto the left renal artery. Using the tail-cuff method, blood pressure of rats was measured before the surgery and at the end of the post-surgical 3rd and 12th weeks. Nicorandil (4mg/kg, orally) or vehicle was administered for 9 weeks. Twelve weeks after RVH surgery, a new object recognition test was performed. Following the determination of blood brain barrier integrity, serum samples were taken for the evaluation of proinflammatory cytokines tumor necrosis alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta). Levels of sodium-potassium adenosine triphosphatase (Na+/K+-ATPase), as a marker of endothelial damage, were evaluated in the hippocampal tissues. RVH resulted in significant increases in TNF-alpha and IL-1 beta levels and decreases in Na+/K+-ATPase levels, along with impairment in blood brain barrier integrity and memory performance. In the nicorandil treatment group, these indices were reversed back to control levels. The present data demonstrated that nicorandil attenuates RVH-induced memory impairment and blood brain barrier damage in rats with RVH.