Person: ÖZBEYLİ, DİLEK
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ÖZBEYLİ
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DİLEK
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Publication Metadata only 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, DilekIntroduction: 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.Publication Metadata only NESFATIN-1 PROTECTS FROM ACUTE PANCREATITIS: ROLE OF MELANOCORTIN RECEPTORS(POLISH PHYSIOLOGICAL SOC, 2019) ÖZBEYLİ, DİLEK; Buzcu, H.; Ozbevli, D.; Yuksel, M.; Kava, O. T. Cilingir; Cakir, O. KasimavNesfatin-1, a recently discovered peptide, was shown to have anti-inflammatory effects. Acute pancreatitis (AP) is a life-threatening condition caused by various reasons. Although the etiology of AP is well-known, its pathogenesis is not clear. The aim of this study is to investigate the possible anti-inflammatory role of nesfatin-1 and its probable protective underlying mechanisms in an acute pancreatitis model. Caerulein was applied intraperitoneally to induce acute pancreatitis in Sprague-Dawley female rats. Nesfatin-1 was administered 5 minutes before the application of caerulein to determine its potential anti-inflammatory role on AP. Five minutes before nesfatin-1 injection, in order to investigate the underlying mechanism, oxytocin receptor antagonist (atosiban), melanocortin receptor antagonist (HS024), or ghrelin receptor antagonist (cortistatin) were administered. Five minutes after nesfatin-1 administration, two doses of caerulein were applied one hour apart. The rats were sacrified 12 hours after the first caerulein dose for serum and pancreatic tissue sampling. Microscopic damage scoring, malondialdehyde and glutathione levels, myeloperoxidase activity, luminol and lucigenin chemiluminescence levels in pancreatic tissue and amylase, lipase, trypsinogen-2 levels in serum were evaluated. Oxidative damage was decreased with nesfatin-1 treatment in the acute pancreatitis model (P < 0.05 - 0.001). The administration of HS024 reversed the effect of nesfatin-1, via increasing lipase, amylase, trypsinogen-2, malondialdehyde (MDA), myeloperoxidase (MPO) and lucigenin levels (P < 0.05 - 0.01). Atosiban pre-treatment elevated MPO activity, luminol and lucigenin chemiluminescence levels (P < 0.01 - 0.001) and cortistatin increased lucigenin and luminol chemiluminescence (P < 0.05 - 0.01). Although receptor antagonists reversed the effect of nesfatin-1 on related biochemical parameters, no significant difference was found in histological scoring. Our results indicated that nesfatin-1 had an anti-inflammatory effect on acute pancreatitis via mainly effecting melanocortin receptors.Publication Metadata only Protective effect of alpha-lipoic acid, aerobic or resistance exercise from colitis in second hand smoke exposed young rats(WILEY, 2017) AKAKIN, DİLEK; Ozbeyli, Dilek; Berberoglu, Ayse Cansu; Ozen, Anil; Erkan, Oktay; Basar, Yunus; Sen, Tunahan; Akakin, Dilek; Yuksel, Meral; Cakir, Ozgur KasimayThe role of second hand smoke (SHS) exposure on ulcerative colitis is not known. Our aim was to examine the effects of -lipoic acid (ALA), chronic aerobic (AE) or resistance exercise (RE) on SHS exposed rats with colitis. Sprague-Dawley male rats (150-200g, n=54) were selected for colitis induction. Among the colitis groups, one group was exposed to SHS (6d/wk, 4cigarettes/d) and the other was not. The SHS group was divided into subgroups as follows: sedentary; AE (swimming; 3d/wk); and RE (climbing with weight; 3d/wk). After 5weeks, colitis was induced by intrarectal acetic acid. All groups had subgroups that were given subcutaneously ALA (50mg/kg per day) or vehicle for 3days. Following decapitation, colon tissues were sampled to examine malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity, luminol and lucigenin chemiluminenscence, macroscopic scoring and histologic examination. ANOVA and Student's t-test were used for statistical analysis. The increased macroscopic and microscopic scores, MPO, MDA, luminol and lucigenin measurements in colitis and SHS-colitis groups were decreased via ALA (P<.05-.001). AE declined macroscopic and microscopic scores, MDA, lucigenin compared to colitis and SHS-colitis groups (P<.01-.001). RE reduced microscopic score, MPO, MDA, luminol, lucigenin (P<.05-.001) that were increased with colitis. Decreased GSH levels (P<.01) in the SHS-colitis group approached to control levels when given ALA. According to our results SHS and colitis induction increased inflammatory damage. SHS did not worsen it more than colitis. Our results suggest that ALA, AE or RE might be protective for SHS exposed ulcerative colitis conditions.