Person: AYDIN OMAY, BANU
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AYDIN OMAY
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Publication Open Access The behavioral and neurochemical effects of methylprednisolone or metyrapone in a post-traumatic stress disorder rat model(KARE PUBL, 2019) AYDIN OMAY, BANU; Tanriverdi, Ayse Melek; Aydin, Banu; Bebitoglu, Berna Terzioglu; Cabadak, Hulya; Goren, M. ZaferOBJECTIVE: Mechanisms contributing to the post-traumatic stress disorder (PTSD) that involve several physiological sys- tems, and the activation of the hypothalamic-pituitary-adrenal axis (HPA) is one of the most known systems in the PTSD pathophysiology. The present study investigates the potential effects of methylprednisolone, metyrapone and their association with the noradrenergic system within the rostral pons, a region containing the locus coeruleus (LC) in a rat model of PTSD induced with predator scent. METHODS: In this study, Sprague-Dawley rats were exposed to the stress by exposure to the scent of dirty cat litter, which is a natural stressor of a predator. One week later, the rats were re-exposed to a situational reminder (clean cat litter). The rats were treated using either methylprednisolone, metyrapone or physiological saline before exposure to a situational reminder (n=8 in each group). Noradrenaline (NA) levels in the rostral pons homogenates were analysed using ELISA. RESULTS: The anxiety indices of the rats exposed to the trauma were found to be significantly higher than the anxiety indices of the control rats. Metyrapone produced a significant increase in the anxiety indices of the non-stressed rats, and methylprednisolone did not produce a change in the anxiety indices of the non-stressed rats. Methylprednisolone treatment suppressed the anxiety in the stressed rats. Metyrapone treatment increased the anxiety indices in the stressed rats but still being lower than that of the saline-treated stressed rats. Significant decrease in the freezing time was observed following the methylprednisolone treatment both in the stressed and non-stressed rats. NA content in the rostral pons of the stressed rats was significantly higher than that of the non-stressed rats. Methylprednisolone or metyrapone treatments decreased the NA content in the non-stressed rats as compared to the saline treatment. However, these decreases were not significant. CONCLUSION: In this study, findings suggest that stress may give rise to endocrine, autonomic and behavioural responses. The anxiety indices and NA levels in the rostral pons increased with the traumatic event. The methylprednisolone treatment may suppress anxiety through interactions between the LC and the HPA axis.Publication Open Access The role of Glu N1 activated nitric oxide synthase in rat model of post traumatic stress disorder(2016-01-01) AYDIN OMAY, BANU; CABADAK, HÜLYA; GÖREN, MEHMET ZAFER; ayhan B. G., AYKAÇ A., gür k., AYDIN B., Seçgin E., Seven İ., CABADAK H., GÖREN M. Z.Objectives: Activation of neuronal nitric oxide synthase (nNOS) and interrelated alterations of calmodulin and ionotropic glutamate receptor (GluN1) levels are unknown in post traumatic stress disorder (PTSD). Materials and Methods: Sprague-Dawley rats of both sexes were exposed to to dirty cat litter, and then placed on an elevated plus maze. An anxiety index was calculated and tissue samples from hippocampus and amygdala were prepered in order to to detect calmodulin, NOS and GluN1 by immunoblotting. Results: The anxiety indices of the traumatized rats were markedly higher than those of the controls (p<0.05). GluN1 and calmodulin levels were decreased in the dorsal hippocampus and amygdaloid complex of the traumatized rats. NOS expression increased significantly in both the amygdaloid complex and dorsal hippocampus where the increase was statistically more prominent in the amygdaloid complex (p< 0.001) than in the dorsal hippocampus of the traumatized rats (p<0.05). Conclusion: Predator exposure in rats causes long-lasting anxiogenic effects associated with increases in NOS and decreases in GluN1 expressions in brain areas related to PTSD symptoms and excitotoxicity. The results suggest that excitotoxicity occurs through other mechanisms rather than GluN1 receptors. Keywords: Predator scent test, nNOS, Glutamate, Calmodulin, Amygdala, HippocampusPublication Open Access Effects of carbachol on apoptosis in human chronic myelogenous leukemic K562 cell line(MARMARA UNIV, FAC MEDICINE, 2019-01-31) AYDIN OMAY, BANU; Aydin, Banu; Tulunay, Aysin; Eksioglu-Demiralp, Emel; Kan, Beki; Cabadak, HulyaObjectives: Muscarinic receptors mediate diverse actions of acetylcholine in the central nervous system and in non-nervous tissues innervated by the parasympathetic nervous system. Our study aims to evaluate the potential association of the M-3 muscarinic receptor with K562 cell proliferation and death. Materials and Methods: Cell proliferation was evaluated by bromodeoxyuridine (BrDU) incorporation. To show early, late apoptosis and cell death, cells were labelled with Annexin V, propidium iodide (PI) and analyzed by flow cytometry. Nuclear extracellular signal-regulated kinase (ERK/pERK) expression was measured by western blot analysis. Results: Treatment with carbachol (CCh) for 48h decreased cell number. Exposing K562 cells to CCh for 24h decreased the number of early apoptotic cells but did not change the number of late apoptotic and necrotic cells. CCh treatment for 48h increased the number of necrotic cells, but decreased the number of early and late apoptotic cells. In response to CCh, nuclear ERK expression was increased and this effect was reversed by 1,1-dimethyl-4-diphenylacetoxypiperidinium iodide (4DAMP). Nuclear pERK expression was decreased in CCh treated cells, 4DAMP did not reverse the effect. Conclusion: Our data suggest that cholinergic agonist CCh affects cell proliferation in K562 cells not only through muscarinic receptors but also through other cholinergic receptors.Publication Open Access Effects of cholinergic compounds and TNF-alpha on human erythroleukemia K562 cell proliferation and caspase expression(MARMARA UNIV, FAC MEDICINE, 2019-01-31) AYDIN OMAY, BANU; Kanli, Zebra; Aydin, Banu; Cabadak, HulyaObjective: The purpose of this study was to investigate if stimulating auto-paracrine muscarinic receptor signalling pathway could change human erythroleukemia K562 cell proliferation and caspase 3, 8 and 9 expression levels. To better understand the role of muscarinic receptors in cell signalling mechanism, we investigated the effects of several compounds on human erythroleukemia K562 cell proliferation and caspase 3, 8 and 9 expression. These compounds were M-3 muscarinic receptor agonist, pilocarpine, pro-inflammatory cytokine, tumor necrosis factor (TNF)-alpha, and the wortmannin which is a phosphoinositide 3-kinase inhibitor. Materials and Methods: Cell proliferation and cell viability were evaluated by the trypan blue exclusion test and 5-Bromo-2-deoxy-uridine (BrdU) Labelling and Detection Kits. Caspase 3, 8 and 9 expression levels were determined by immunoblot analysis. Results: Both pilocarpine and TNF-alpha caused a small increase in human erythroleukemia K562 cell proliferation. However, when all the compounds were treated together, proliferation of human erythroleukemia K562 cells increased significantly when compared to untreated control cells. TNF-alpha and wortmannin treatment increased caspase 3 and caspase 8 expression patterns significantly in human erythroleukemia K562 cells. TNF-alpha and wortmannin treatment increased caspase 9 expression level (P>0.05) but it was not significant. Conclusion: These findings partly demonstrated that M-3 muscarinic receptor mediated an increase in K562 cell proliferation. Pilocarpine prevented TNF-alpha and wortmannin induced caspase 3 and 8 expression and indirectly showed apoptosis in human erythroleukemia K562 cells.