Person: AKAKIN, DİLEK
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AKAKIN
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DİLEK
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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 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.Publication Metadata only Neuropeptide-w protects against stress-induced gastric ulcer in rats via the involvement of capsaicin-sensitive vagal afferent fibers(2020-11-28) PEKER EYÜBOĞLU, İREM; AKKİPRİK, MUSTAFA; YEGEN, BERRAK; AKAKIN, DİLEK; ARABACI TAMER S., AKBULUT S., AKAKIN D., PEKER EYÜBOĞLU İ., AKKİPRİK M., YEGEN B.AIM: Neuropeptide-W (NPW), expressed in hypothalamus and peripheral organs, activates hypothalamus-pituitary-adrenal axis, and may have a physiological role in neuroendocrine response to stress. The aim was to evaluate protective effects of NPW on stress-induced gastric injury in rats. METHODS: Sprague-Dawley male rats were fasted for 24 hours, restrained and immersed in water-bath for 6 h to induce water-immersion restraint stress (WIRS), and NPW (0.1 or 5µg/kg) or saline was injected subcutaneously at 15 minutes before WIRS (n=24), while saline-injected control rats had no WIRS (n=8). For degeneration of vagal afferent fibers (VAD), in some rats (n=24) capsaicin (1%) was applied perivagally under ketamine anesthesia, and 3 weeks later WIRS was induced. Using a laser Doppler, gastric serosal blood flow was monitored under anesthesia. Following cardiac puncture, gastric tissues were removed for macroscopic/microscopic scoring and measurement of myeloperoxidase activity, malondialdehyde and glutathione levels. Gastric NF-κB and cerebral NPW mRNA expressions were detected by RT-PCR. One-way ANOVA was used for statistical analysis. RESULTS: WIRS decreased mean serosal blood flow, resulted in elevated macroscopic/ microscopic scores compared to control group (p<0.001), while myeloperoxidase activity and malondialdehyde level were elevated (p<0.05) and antioxidant glutathione was depleted (p<0.001). WIRS depressed gastric NF-κB and cerebral NPW mRNA expressions (p<0.01). Neither doses of NPW changed gastric NF-κB mRNA. Lowerdose of NPW elevated blood flow (p<0.001), abolished WIRS-induced elevations in myeloperoxidase and malondialdehyde levels (p<0.05). High-dose NPW replenished gastric glutathione and brain NPW expression and reduced scores (p<0.05-0.01). Despite that VAD did not alter effects of high-dose NPW, reductions in malondialdehyde and myeloperoxidase, and improvement in blood flow by low-dose NPW were abolished by VAD (p<0.05). CONCLUSION: In stress-induced oxidative gastric injury, NPW provides gastroprotection by improving depressed blood flow and inhibiting ulcer-induced oxidative injury, which involve contribution of vagal afferent fibers