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AKAKIN, DİLEK

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    PublicationOpen Access
    Ethanol extract of Cotinus coggygria leaves accelerates wound healing process in diabetic rats
    (TAYLOR & FRANCIS LTD, 2016-11) ŞEN, ALİ; Aksoy, Halil; Sen, Ali; Sancar, Mesut; Sekerler, Turgut; Akakin, Dilek; Bitis, Leyla; Uras, Fikriye; Kultur, Sukran; Izzettin, Fikret Vehbi
    Context:Cotinus coggygria Scop. (Anacardiaceae) leaves that were used as wound healing in traditional Balkan and Anatolian folk medicine, could be potentially effective in treating diabetic wounds.Objective: This study investigates biochemical and histological effects of ethanol extract of C. coggygria (CCE) on excision wound model in diabetic rats.Materials and methods: This study was conducted on diabetic Wistar albino rats, which were injected by a single dose (50mg/kg i.p.) streptozotocin. Afterward an excision wound model was created in all animals; diabetic control rats were applied topically simple ointment and diabetic treatment rats were applied topically 5% (w/w) ointment with CC, once a day during the experimental period. Malondialdehyde, glutathione and hydroxyproline levels in wound tissues were investigated at the end of 3rd, 7th, and 14th days. Histopathological examination was also performed.Results: Hydroxyproline content was significantly increased in the CCE treated group versus control after the 3rd and 7th days (15.33 versus 11.83; 19.67 versus 15.67mg/g, p<0.05; respectively). A statistically significant elevation in glutathione at the end of 3rd, 7th, and 14th days (5.13 versus 1.58, p<0.05; 4.72 versus 1.88, p<0.05; 3.83 versus 1.88mol/g, p<0.05, respectively) and a statistically significant decrease in malondialdehyde level at the end of 7th day (4.49 versus 1.48nmol/g, p<0.05) were determined in the treated group versus control group. These results were also supported by histological analyses.Discussion and conclusion: These findings indicate that CCE accelerated the cutaneous wound healing process in diabetic wounds, in confirmation of its traditional use.
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    Protective effect of low dose caffeine on psychological stress and cognitive function
    (PERGAMON-ELSEVIER SCIENCE LTD, 2017) AKAKIN, DİLEK; Cakir, Ozgur Kasimay; Ellek, Nurfitnat; Salehin, Nabila; Hamamci, Rabia; Keles, Hulya; Kayali, Damla Gokceoglu; Akakin, Dilek; Yuksel, Meral; Ozbeyli, Dilek
    Introduction: Caffeine is an adrenergic antagonist that enhances neuronal activity. Psychological stress depresses cognitive function. Aim: To investigate the effects of acute and chronic low dose caffeine on anxiety-like behavior and cognitive functions of acute or chronic psychological stressed rats. Material-method: Acute or chronic caffeine (3 mg/kg) was administered to male Sprague Dawley rats (200-250 g, n = 42) before acute (cat odor) and chronic variable psychological stress (restraint overcrowding stress, elevated plus maze, cat odor, forced swimming) induction. Anxiety and cognitive functions were evaluated byhole-board and object recognition tests. The brain glutathione and malondialdehyde assays, myeloperoxidase, nitric oxide (NO), superoxide dismutase (SOD), luminol and lucigenin activity and histological examination were done. ANOVA and Student's t-test were used for statistical analysis. Results: The depressed cognitive function with chronic stress exposure and the increased anxiety-like behavior with both stress inductions were improved via both caffeine applications (p < 0.05-0.001). Both caffeine pretreatments in chronic stressed rats, and chronic caffeine in acute stressed ones reduced the elevated myeloperoxidase activities (p < 0.05-0.01). The increased malondialdehyde, lucigenin and NO levels with acute stress were inhibited with chronic caffeine (p < 0.05-0.01), malondialdehyde and NO levels were declined by acute caffeine (p < 0.001). Acute caffeine decreased SOD activity (p < 0.01) and improved glutathione (p < 0.01) and luminol levels (p < 0.05). The induced histological damage with both stress exposures was ameliorated with chronic caffeine. Conclusion: The increased anxiety-like behavior and depleted cognitive functions under stress conditions were improved with both acute and predominantly chronic caffeine pretreatments by decreasing oxidative damage parameters. (C) 2016 Elsevier Inc. All rights reserved.
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    Three dimensional anatomical microdissection of rat brain using fiber dissection technique
    (WOLTERS KLUWER MEDKNOW PUBLICATIONS, 2014) AKAKIN, DİLEK; Akakin, A.; Yilmaz, B.; Akakin, D.; Dagbasi, N.; Kilic, T.
    Introduction: Using Klingler's fiber dissection technique, we aimed to demonstrate micro-dissections of the specific regions in the brain of rat which is undoubtly one of the mostly used animal in neuroscience researches. Methods: Formalin fixed cerebral hemispheres of rat brains were dissected under operating microscope. Klingler's technique of fiber dissection was applied. Cortex, intrinsic anatomy and cranial nerves were studied. During and after dissection, photographs were taken and three dimensional pictures were obtained using a special software (Anamaker 3D; available free from wwi.v.stereoeye.com, Tokyo, Japan). Results: The anatomical relation of structures, seen in histological sections, was determined in our study. Hippocampus, thalamus and internal capsule, which are frequently studied, are explained with three dimensional fiber dissection technique. In rats, trigeminal nerve, olfactory nerve, hippocampus lying to the fornix and olfactory bulb lying to the frontal horn are more distinct when compared to humans. Discussion: The microdissection of rat brain, to obtain needed structures accurately for experimental purposes, is an extremely important model. On this basis, our study serves the microsurgical anatomy of the rat brain for neuroscientists knowledge. Copyright (C) 2014, Anatomical Society of India. Published by Reed Elsevier India Pvt. Ltd. All rights reserved.
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    PublicationOpen Access
    Effects of montelukast sodium on tendon healing: An experimental study
    (SPRINGER HEIDELBERG, 2013) AKAKIN, DİLEK; Polat, Atilla; Canbora, Mehmet Kerem; Akakin, Dilek; Aykanat, Faruk
    Introduction: Montelukast sodium (MS) a selective leukotriene antagonist of the cysteinyl leukotriene receptor, has been used in the treatment of asthma and allergic rhinitis. In this study, we evaluated the effect of MS on the early inflammatory phase (histological) of nonsynovial tendon healing. Materials and Methods: Rats were divided randomly into two groups (n = 6 each). MS (Singulair) was administered to one group at 10 mg/kg/day [250 g/day intraperitoneally (i.p.)]. The control group was administered 250 g/day of 0.9% saline i.p. This nonsynovial tendon was longitudinally divided at the midportion, cut transversely and then sutured. In both groups, the rats were sacrificed by decapitation 10 days later. Results: Decreased inflammatory cell infiltration and more properly oriented collagen fibres were observed in the MS group's histopathological specimens as compared to the control group's (P < 0.05). Additionally, vascularity was decreased in the MS group. Conclusion: MS decreased tendon healing, apparently by inhibiting the early inflammatory phase of nonsynovial tendon healing.
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    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.
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    Ameliorative Effect of Chronic Moderate Exercise in Smoke Exposed or Nicotine Applied Rats From Acute Stress
    (OXFORD UNIV PRESS, 2015) YARAT, AYŞEN; Kuru, Pinar; Bilgin, Seyda; Mentese, Semih Tiber; Tazegul, Gokhan; Ozgur, Sevinc; Cilingir, Ozlem T.; Akakin, Dilek; Yarat, Aysen; Kasimay, Ozgur
    Introduction: Physical activity has been found to be related with many health benefits. Our aim was to investigate the effect of chronic moderate exercise from acute stress on nicotine and cigarette smoke exposed rats. Methods: Male Sprague Dawley rats (200-250 g, n = 48) were divided into 6 groups as non-exercised, exercised, smoke exposed, smoke exposed and exercised, nicotine applied, and nicotine applied and exercised. Nicotine bitartarate was applied intraperitoneally (0.1 mg/kg/day) for 5 weeks, and cigarette smoke was exposed in a ventilated chamber. After 1 week of nicotine application or smoke exposure, moderate exercise training protocol was applied to exercise groups. At the end of the experiments, acute stress induction was made to all groups by electric foot shock. Holeboard tests were performed before and after the experiments. Biochemical and histological analyses were performed in lung, liver, colon, stomach, and gastrocnemius tissues. Results: Malondialdehyde levels were increased in all tissues of smoke exposed group (p < .05-.01) except gastrocnemius tissue compared to non-exercised group and were decreased with exercise (p < .05-.001). Myeloperoxidase levels were increased in lung, liver and colon tissues of smoke exposed group (p < .05-.001) and liver and colon tissues of nicotine applied rats (p < .01-.001) and decrease with exercise in liver and colon tissues of both smoke exposed or nicotine applied groups (p < .05-.01). In all tissue samples, increased histological injury scores (p < .05-.001) decreased significantly with exercise (p < .01-.001). Conclusion: Biochemical parameters and histological scoring indicated increased tissue injury due to nicotine application and cigarette smoke exposure and exercise training ameliorated these effects in most of the tissues of acute stress induced rats.
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    Melatonin improves hyperglycemia induced damages in rat brain
    (WILEY, 2018) YARAT, AYŞEN; Gurel-Gokmen, Begum; Ipekci, Hazal; Oktay, Sehkar; Alev, Burcin; Ustundag, Unsal Veli; Ak, Esin; Akakin, Dilek; Sener, Goksel; Emekli-Alturfan, Ebru; Yarat, Aysen; Tunali-Akbay, Tugba
    Background Diabetes mellitus is an endocrine disorder which is characterized by the development of resistance to the cellular activity of insulin or inadequate insulin production. It leads to hyperglycemia, prolonged inflammation, and oxidative stress. Oxidative stress is assumed to play an important role in the development of diabetic complications. Melatonin is the hormone that interacts with insulin in diabetes. Therefore, in this study, the effects of melatonin treatment with or without insulin were examined in diabetic rat brain. Methods Results Rats were divided into five groups as control, diabetes, diabetes + insulin, diabetes + melatonin, and diabetes + melatonin + insulin. Experimental diabetes was induced by streptozotocin (60 mg/kg, i.p.). Twelve weeks after diabetes induction, rats were decapitated. Malondialdehyde, glutathione, sialic acid and nitric oxide levels, superoxide dismutase, catalase, glutathione-S-transferase, myeloperoxidase, and tissue factor activities were determined in brain tissue. Melatonin alone showed its antioxidant effect by increasing brain glutathione level, superoxide dismutase, catalase, and glutathione-S-transferase activities and decreasing malondialdehyde level in experimental diabetes. Although insulin did not have a significant effect on glutathione and glutathione-S-transferase, its effects on lipid peroxidation, superoxide dismutase, and catalase were similar to melatonin; insulin also decreased myolopeoxidase activity and increased tissue factor activity. Combined melatonin and insulin treatment mimicked the effects of insulin. Conclusion Addition of melatonin to the insulin treatment did not change the effects of insulin, but the detailed role of melatonin alone in the treatment of diabetes merits further experimental and clinical investigation.
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    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.
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    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, Goksel
    The 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.
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    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, Goksel
    Spinal 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.