Person: AKAKIN, DİLEK
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AKAKIN
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DİLEK
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Publication Metadata only Functional and structural changes of the urinary bladder following spinal cord injury; treatment with alpha lipoic acid(WILEY, 2017) VELİOĞLU ÖĞÜNÇ, AYLİZ; Ekiz, Arif; Ozdemir-Kumral, Zarife Nigar; Ersahin, Mehmet; Tugtepe, Halil; Ogunc, Ayliz Velioglu; Akakin, Dilek; Kiran, Demir; Ozsavci, Derya; Biber, Necat; Hakan, Tayfun; Yegen, Berrak C.; Sener, Goksel; Toklu, Hale Z.BACKGROUND & AIMAlpha lipoic acid (LA) was shown to exert neuroprotection in trauma-induced spinal cord injury (SCI), which is frequently associated with urinary bladder complaints in patients with SCI. Accordingly, the protective effects of LA on biochemical and histological changes in bladder as well as functional studies were assessed. METHODSWistar albino rats were divided as control, SCI, and LA (50mg/kg/day, ip) treated SCI groups (SCI+LA). The standard weight-drop (100g/cm force at T10) method was used to induce a moderately severe SCI. One week after the injury, neurological examination was performed and the rats were decapitated. Bladder samples were taken for histological examination, functional (isolated tissue bath) studies, and for the measurement of biochemical parameters (malondialdehyde, MDA; gluthathione, GSH; nerve growth factor, NGF; caspase-3, luminol and lucigenin chemiluminescences). RESULTSSCI caused a significant (P<0.001) increase in the detrusor muscle thickness. It increased the contractility responses to carbachol and relaxation responses to papaverine (P<0.05-0.001). There were also significant alterations in MDA, caspase-3, luminol, and lucigenin chemiluminescences with concomitant decreases in NGF and GSH (P<0.05). LA treatment reversed histological and functional (contraction and relaxation responses) changes induced by SCI (P<0.05-0.001), but no significant recovery was observed in the impaired neurological functions. CONCLUSIONThese results indicate that LA have a beneficial effect in improving the bladder tonus via its antioxidant and anti-inflammatory actions following SCI.Publication Metadata only The Anti-Inflammatory and Neuroprotective Effects of Ghrelin in Subarachnoid Hemorrhage-Induced Oxidative Brain Damage in Rats(MARY ANN LIEBERT, INC, 2010) VELİOĞLU ÖĞÜNÇ, AYLİZ; Ersahin, Mehmet; Toklu, Hale Z.; Erzik, Can; Cetinel, Sule; Akakin, Dilek; Velioglu-Ogunc, Ayliz; Tetik, Sermin; Ozdemir, Zarife N.; Sener, Goeksel; Yegen, Berrak C.To elucidate the putative neuroprotective effects of ghrelin in subarachnoid hemorrhage (SAH)- induced brain injury, Wistar albino rats (n=54) were divided into sham-operated control, saline-treated SAH, and ghrelin-treated (10 mu g/kg/d IP) SAH groups. The rats were injected with blood (0.3mL) into the cisterna magna to induce SAH, and were sacrificed 48 h after the neurological examination scores were recorded. In plasma samples, neuron-specific enolase (NSE), S-100 beta protein, TNF-alpha, and IL-1 beta levels were evaluated, while forebrain tissue samples were taken for the measurement of malondialdehyde (MDA), glutathione (GSH), reactive oxygen species levels, myeloperoxidase (MPO), Na+-K+-ATPase activity, and DNA fragmentation ratio. Brain tissue samples containing the basilar arteries were obtained for histological examination, while cerebrum and cerebellum were removed for the measurement of blood-brain barrier (BBB) permeability and brain water content. The neurological scores were impaired at 48 h after SAH induction, and SAH caused significant decreases in brain GSH content and Na+-K+-ATPase activity, and increases in chemiluminescence, MDA levels, and MPO activity. Compared with the control group, the protein levels of NSE, S-100 beta, TNF-alpha, and IL-1 beta in plasma were also increased, while ghrelin treatment prevented all SAH-induced alterations observed both biochemically and histopathologically. The results demonstrate that ghrelin alleviates SAH-induced oxidative brain damage, and exerts neuroprotection by maintaining a balance in oxidant-antioxidant status, by inhibiting proinflammatory mediators, and preventing the depletion of endogenous antioxidants evoked by SAH.Publication Metadata only The effects of Nigella sativa against oxidative injury in a rat model of subarachnoid hemorrhage(SPRINGER WIEN, 2011) YEGEN, BERRAK; Ersahin, Mehmet; Toklu, Hale Z.; Akakin, Dilek; Yuksel, Meral; Yegen, Berrak C.; Sener, GokselThe aim of the study was to investigate the putative neuroprotective effect of Nigella sativa oil (NSO) treatment against subarachnoid hemorrhage (SAH) in rats. To induce SAH, rats were injected with 0.3 ml blood into their cisterna magna. Male Wistar albino rats were divided as control, vehicle-treated SAH, and NSO-treated (0.2 ml/kg, intraperitoneally) SAH groups. Forty-eight hours after SAH induction, neurological examination scores were recorded and the rats were decapitated. Brain tissue samples were taken for blood brain barrier permeability, brain water content, or determination of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO), and Na+-K+-ATPase activities. On the second day of SAH induction, neurological examination scores were increased in SAH groups, while SAH caused significant decreases in brain GSH content and Na+-K+-ATPase activity, which were accompanied with significant increases in MDA levels and MPO activity. The histological observation showed vasospasm of the basillary artery. On the other hand, NSO treatment markedly improved the neurological scores while all oxidant responses were prevented, implicating that NSO treatment may be of therapeutic use in preventing oxidative stress due to SAH.Publication Metadata only Montelukast inhibits caspase-3 activity and ameliorates oxidative damage in the spinal cord and urinary bladder of rats with spinal cord injury(ELSEVIER SCIENCE INC, 2012) ŞENER, AZİZE; Ersahin, Mehmet; Cevik, Ozge; Akakin, Dilek; Sener, Azize; Ozbay, Latif; Yegen, Berrak C.; Sener, GokselSpinal cord injury (SCI) leads to an inflammatory response that generates substantial secondary damage within the tissue besides the primary damage. Leukotrienes are biologically active 5-lipoxygenase products of arachidonic acid metabolism that are involved in the mediation of various inflammatory disorders including SCI. In this study, we investigated the possible protective effects of montelukast, a leukotriene receptor blocker, on SCI-induced oxidative damage. Wistar albino rats (n = 24) were divided randomly as control, vehicle- or montelukast (10 mg/kg, ip)-treated SCI groups. To induce SCI, a standard weight-drop method that induced a moderately severe injury at T10 was used. Vehicle or montelukast were administered to the injured animals 15 min after injury. At seven days post-injury, neurological examination was performed and rats were decapitated. Blood samples were taken to evaluate leukotriene 134 levels, and pro-inflmamatory cytokines (TNF-alpha, IL-1 beta) while in spinal cord and urinary bladder samples malondialdehyde (MDA), glutathione (GSH), luminol chemiluminescence (CL) levels and myeloperoxidase (MPO) and caspase-3 activities were determined. Tissues were also evaluated histologically. SCI caused significant decreases in tissue GSH, which were accompanied with significant increases in luminol CL and MDA levels and MPO and caspase-3 activities, while pro-inflammatory cytokines in the plasma were elevated. On the other hand. montelukast treatment reversed these parameters and improved histological findings. In conclusion, SCI caused oxidative tissue injury through the activation of pro-inflammatory mediators and by neutrophil infiltration into tissues, and the neuroprotective and antiapoptotic effects of montelukast are mediated by the inhibition of lipid peroxidation, neutrophil accumulation and proinflammatory cytokine release. Moreover, montelukast does not only exert antioxidant and antiapoptotic effects on the spinal cord, but it has a significant impact on the bladder tissue damage secondary to SCI. (C) 2012 Elsevier Inc. All rights reserved.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 Intravesical hyaluronic acid treatment improves bacterial cystitis and reduces cystitis-induced hypercontractility in rats(WILEY, 2015) YEGEN, BERRAK; Yildiz, Nurdan; Alpay, Harika; Tugtepe, Halil; Kumral, Zarife Nigar Ozdemir; Akakin, Dilek; Ilki, Arzu; Sener, Goksel; Yegen, Berrak C.ObjectiveTo investigate the effect of intravesical hyaluronic acid on Escherichia coli-induced cystitis and cystitis-induced hypercontractility in rats. MethodsBacterial cystitis was induced in Wistar female rats by intravesical inoculation of E.coli. Isotonic saline was instilled in the control group (n=6). The rats were either non-treated, treated with gentamycin (4mg/kg, 5days) or treated intravesically with hyaluronic acid (0.5mL, 0.5%). On the eighth day, the bladder tissues were excised for histological examination, and the measurements of myeloperoxidase, superoxide dismutase and catalase activities. Contraction/relaxation responses to carbachol, isoprotrenol and papaverine were studied. ResultsTissue myeloperoxidase activity was increased, but superoxide dismutase and catalase activities were decreased in bacterial cystitis, while hyaluronic acid treatment reversed these changes. In the hyaluronic acid-treated group, healing of the uroepithelium was observed, while decreased inflammatory cell infiltration was obvious in gentamycin-treated group. E.coli-induced cystitis in all rats resulted in increased contraction responses to carbachol compared with controls (P<0.01). Treatment with hyaluronic acid, but not gentamycin, significantly (P<0.05) depressed hypercontractility at maximum carbachol concentrations. In all rats with cystitis, papaverine-induced relaxation was increased, whereas isoproterenol-induced relaxation curves were not different between the studied groups. ConclusionGentamycin treatment, despite its ameliorative effect on inflammation, had no impact on the contractile dysfunction of the injured bladder. Intravesical hyaluronic acid, in addition to its supportive role in the healing of the epithelium, seems to lower the increased threshold for contraction and to reduce oxidative stress. These findings support a potential role for hyaluronic acid in the treatment of bacterial cystitis.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 Metadata only Protective effects of melatonin against spinal cord injury induced oxidative damage in rat kidney: A morphological and biochemical study(ELSEVIER GMBH, 2013) YEGEN, BERRAK; Akakin, Dilek; Kiran, Demir; Ozkan, Naziye; Ersahin, Mehmet; Ozdemir-Kumral, Zarife Nigar; Yegen, Berrak; Sener, GokselSpinal cord injury (SCI) induced oxidative stress affects multiple organ systems including the kidney. We studied the possible protective effects of melatonin on SCI-induced oxidative damage in renal tissues of rats. Wistar albino rats (n =24) were exposed to SCI and divided into vehicle- or melatonin-treated SCI groups. Melatonin was administred intraperitoneally at a dose of 10 mg/kg for seven days. Renal tissues were investigated by light and electron microscopy. Furthermore, tissue malondialdehyde (MDA) and glutathione (GSH) levels and myeloperoxidase (MPO) and superoxide dismutase (SOD) activities were also determined. In the vehicle-treated SCI group, the renal histology was disturbed compared to controls, whereas the melatonin-treated SCI group showed significantly reduced degeneration of renal tissue as seen by both light and electron microscopy. MDA levels, MPO and SOD activities were increased and GSH levels were decreased in the vehicle-treated SCI group compared to controls. On the other hand, decreased MDA levels and MPO activities and increased GSH levels were observed in the melatonin-treated SCI group compared to vehicle-treated SCI group. These results showed that experimentally induced SCI caused oxidative stress in the rat kidney, whereas melatonin treatment reduced oxidative stress, suggesting that it may be used as a complementary therapy of renal problems occurring following SCI. (C) 2013 Elsevier GmbH. All rights reserved.Publication Metadata only Parkinson hastalığı sıçan modelinde ghrelinin gastrointestinal fonksiyon bozukluğu üzerine etkileri(2018-05-23) GÜLHAN, REZZAN; YEGEN, BERRAK; AKAKIN, DİLEK; KARAGÖZ KÖROĞLU A., ANIL D., ARABACI TAMER S., GÜLHAN R., YEGEN B., AKAKIN D.AMAÇ: Gastrointestinal bozukluklar Parkinson hastalarında sıklıkla gözlenmektedir. Bu çalışmada, sıçanlarda 6-hidroksidopamin (6-OHDA) ile indüklenen Parkinson Hastalığı (PH) modelinde antiinflamatuvar etkileri olduğu bilinen ghrelinin mide-kolon motilitesi ve myenterik pleksus vazoaktif intestinal peptit (VIP) ve nöronal nitrik oksit sentaz (nNOS) immünohistokimyası üzerine etkilerini incelemek amaçlanmıştır. GEREÇ VE YÖNTEM: Çalışmada erkek Wistar albino sıçanlar 4 gruba ayrıldı: Yalancı-opere -kontrol-, 6-OHDA, Ghrelin-Ghr- ve 6-OHDA+Ghr grupları (tüm gruplarda n=12). 6-OHDA infüzyonu stereotaksik yöntemle uygulandı. Ghrelin ve 6-OHDA+Ghr grubundaki hayvanlara 4 hafta süreyle 10 ng/kg ghrelin subkutan olarak uygulandı. Deney sonunda hayvanların apomorfin ile indüklenmiş dönme davranışı, fekal atılım ve ağırlıkları değerlendirildi. Dekapite edilen hayvanlarda gastrik motilite tayini yapıldı. Paraformaldehit (%4) perfüzyonu yapılan sıçanlardan beyin, mide ve kolon dokuları elde edildi. Beyin doku kesitlerine tirozin hidroksilaz (TH) immünohistokimyası, mide ve kolon doku kesitlerine Hematoksilen-Eosin boyası ile VIP/nNOS immünohistokimyası uygulandı. Veriler tek yönlü ANOVA ile analiz edildi. BULGULAR: 6-OHDA grubunda kontrol grubuna göre striatumda azalan TH immünreaktivitesi ve gastrik boşalmadaki gecikmenin (p<0,001,p<0,05), ghrelin uygulaması ile arttığı (p<0,001, p<0,01), apomorfin ile indüklenen dönme sayısının azaldığı (p<0,001) gözlendi. 6-OHDA grubunda hayvanların kontrol grubuna göre azalmış olan ağırlıklarının (p<0,001) ghrelin uygulaması ile arttığı izlendi (p<0,05). Kolon myenterik pleksusunda, kontrol grubuna göre 6-OHDA grubunda VIP-immünreaktivitesinin arttığı, nNOS immünreaktivitesinin azaldığı izlendi (p<0,05). Fekal atılım bulgularımıza paralel olarak, 6-OHDA+Ghr grubunda 6-OHDA grubuna göre nNOS immünreaktivitesinin arttığı saptandı (p<0,05). Mide antrumu myenterik pleksusunda kontrole göre 6-OHDA grubunda gözlenen artmış VIP-immünreaktivitesi (p<0,05) ve azalmış nNOS immünreaktivitesinin ghrelin uygulaması ile tersine çevrildiği görüldü (p<0,05). SONUÇ: Ghrelinin 6-OHDA uygulanmış sıçanlarda azalmış gastrointestinal motilite üzerine olumlu etkileri saptanmıştır. Ghrelinin bu etkileri gastrointestinal nörokimyasal plastisite ile ilişkilidir. Bu çalışma Marmara Üniversitesi Bilimsel Araştırma Projeler Komisyonu (BABKO) tarafından desteklenmiştir. SAG-CYLP-131216-0539.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