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AYDIN OMAY, BANU

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AYDIN OMAY

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Start date: 2020 × Has files: true ×

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    PublicationOpen Access
    The Neurochemical Effects of Prazosin Treatment on Fear Circuitry in a Rat Traumatic Stress Model
    (KOREAN COLL NEUROPSYCHOPHARMACOLOGY, 2020-05-31) AYDIN OMAY, BANU; Ketenci, Sema; Acet, Nazife Gokce; Saridogan, Gokce Elif; Aydin, Banu; Cabadak, Hulya; Goren, Mehmet Zafer
    Objective: The timing of administration of pharmacologic agents is crucial in traumatic stress since they can either potentiate the original fear memory or may cause fear extinction depending on the phase of fear conditioning. Brain noradrenergic system has a role in fear conditioning. Data regarding the role of prazosin in traumatic stress are controversial. Methods: In this study, we examined the effects of prazosin and the noradrenergic system in fear conditioning in a predator stress rat model. We evaluated the direct or indirect effects of stress and prazosin on noradrenaline (NA), gamma-aminobuytyric acid (GABA), glutamate, glycine levels and choline esterase activity in the amygdaloid complex, the dorsal hippocampus, the prefrontal cortex and the rostral pons. Results: Our results demonstrated that prazosin might alleviate defensive behaviors and traumatic stress symptoms when given during the traumatic cue presentation in the stressed rats. However prazosin administration resulted in higher anxiety levels in non stressed rats when the neutral cue was presented. Conclusion: Prazosin should be used in PTSD with caution because prazosin might exacerbate anxiety in non-traumatized subjects. However prazosin might as well alleviate stress responses very effectively. Stress induced changes included increased NA and GABA levels in the amygdaloid complex in our study, attributing noradrenaline a possible inhibitory role on fear acquisition. Acetylcholine also has a role in memory modulation in the brain. We also demonstrated increased choline esterase acitivity. Cholinergic modulation might be another target for indirect prazosin action which needs to be further studied.
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    PublicationOpen Access
    Potential antiproliferative and apoptotic effects of pilocarpine combined with TNF alpha in chronic myeloid leukemia cells
    (2023-01-01) CABADAK, HÜLYA; AYDIN OMAY, BANU; Kanlı Z., CABADAK H., AYDIN OMAY B.
    © 2023, The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.Pilocarpine is a selective M1/M3 agonist of muscarinic acetylcholine receptor subtypes. Muscarinic acetylcholine receptors are G protein-coupled receptors. These receptors are different drug targets. The aim of the present work was to investigate the effect of pilocarpine on the expression of M3 muscarinic acetylcholine receptor, the AChE activity, IL-8 release response, and proliferation in K562 cells, via muscarinic receptor activation. Human chronic myeloid leukemic cell cultures were incubated with drugs. Proliferation assays were performed by BrdU assay. Expression of M3 muscarinic acetylcholine receptor and apoptosis proteins such as bcl, bax, cyt C, and caspases was assessed with the semiquantitative Western blotting method. Pilocarpine inhibits chronic myeloid cell proliferation and M3 muscarinic acetylcholine receptor protein expression. Pilocarpine increases caspase-8 and -9 expression levels, upregulating the proapoptotic protein Bax and downregulating the expression levels of the antiapoptotic protein Bcl-2. The apoptotic activity of pilocarpine is associated with an increase in AChE activity. M3 muscarinic acetylcholine receptors can activate multiple signal transduction systems and mediate inhibitory effects on chronic myeloid K562 cell proliferation depending on the presence of 1% FBS conditions. This apoptotic effect of pilocarpine may be due to the concentration of pilocarpine and the increase in AChE level. Our results suggest that inhibition of cell proliferation by inducing apoptosis of pilocarpine in K562 cells may be one of the targets. M3 selective agonist may have therapeutic potential in chronic myeloid leukemia. Graphical Abstract: [Figure not available: see fulltext.].
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    PublicationOpen Access
    The role of epidermal growth factor and cholinergic receptor agonists and antagonists in MAPK signal transduction in K562 cells
    (2023-08-01) AYDIN OMAY, BANU; Atmaca S. G., Aydın Omay B., Cabadak H.
    Objective: Muscarinic receptors (M1-M5) are members of the G protein-coupled receptor superfamily and are effective in physiological functions through G proteins. Recent studies suggested that cholinergic receptors mediate cellular activities in hematopoietic cells. The aim of this study was to investigate the potential role of mitogen-activated protein kinases (MAPK) signaling extracellular signalregulated kinases 1 and 2 (ERK1/2)/phosphorylated ERK1/ (pERK1/2) pathways in chronic myeloid leukemia (K562) cells. Materials and Methods: Chronic myeloid leukemia cells were cultured. Cells were incubated in the presence of muscarinic receptor agonist, antagonist and epidermal growth factor (EGF). To detect MAPK activation, ERK/pERK protein expression levels were determined by western blot method techniques. Results: Our study results showed that cholinergic agents and EGFs affect the MAPK pathway in the human K562 cell line. Conclusion: Cholinergic and EGF receptors may affect the MAPK pathway in K562 cells. Conclusion: Cholinergic and EGF receptors may affect the MAPK pathway in K562 cells.