Person: ARICIOĞLU, FEYZA
Loading...
Email Address
Birth Date
Research Projects
Organizational Units
Job Title
Last Name
ARICIOĞLU
First Name
FEYZA
Name
13 results
Search Results
Now showing 1 - 10 of 13
Publication Open Access Neuroinflammation in Schizophrenia: A Critical Review and The Future(KURE ILETISIM GRUBU A S, 2016-12) ARICIOĞLU, FEYZA; Aricioglu, Feyza; Ozkartal, Ceren Sahin; Unal, Gokhan; Dursun, Serdar; Cetin, Mesut; Mueller, NorbertSchizophrenia is a serious mental illness that affects approximately 1% of the population worldwide, with positive, negative and cognitive dysfunctions and a significant deterioration in psychosocial functioning. Interactions between genetic predisposition and environmental stressors at the early stages of life, and subsequently a molecular level neurodegeneration process are important in the development of schizophrenia. Current approaches suggest that cytokines-induced neuroinflammation might have a role in the development of several psychiatric disorders, including schizophrenia. Uncontrolled microglial activation, increase in pro-inflammatory cytokines, and subsequent neurotransmitter dysfunctions can induce schizophrenia. Microglial activation induced by pro-inflammatory cytokines in central nervous system is responsible for the initiation and proceeding of the inflammatory process and consequently developing neurodegeneration. Here in this review, we aimed to provide an overview to the latest findings related to the cytokines-mediated peripheral and central immune responses in the development of schizophrenia.Publication Open Access Effect of agmatine on the development of morphine dependence in rats: potential role of cAMP system(ELSEVIER, 2004-11) ARICIOĞLU, FEYZA; Aricioglu, F; Means, A; Regunathan, SAgmatine is an endogenous amine derived from arginine that potentiates morphine analgesia and blocks symptoms of naloxone-precipitated morphine withdrawal in rats. In this study, we sought to determine whether treatment with agmatine during the development of morphine dependence inhibits the withdrawal symptoms and that the effect is mediated by cAMP system. Exposure of rats to morphine for 7 days resulted in marked naloxone-induced withdrawal symptoms and agmatine treatment along with morphine significantly decreasing the withdrawal symptoms. The levels of cAMP were markedly increased in morphine-treated rat brain slices when incubated with naloxone and this increase was significantly reduced in rats treated with morphine and agmatine. The induction of tyrosine hydroxylase after morphine exposure was also reduced in locus coeruleus when agmatine was administered along with morphine. We conclude that agmatine reduces the development of dependence to morphine and that this effect is probably mediated by the inhibition of cAMP signaling pathway during chronic morphine exposure. (C) 2004 Elsevier B.V. All rights reserved.Publication Metadata only Neuroprotective effects of agmatine in antineoplastic drugs induced neurotoxicity: In vitro study(PERGAMON-ELSEVIER SCIENCE LTD, 2019) ARICIOĞLU, FEYZA; Binnetoglu, Damla; Hacimuftuoglu, Ahmet; Aricioglu, FeyzaAims: The effects of agmatine, an endogenous substance known to have a neuroprotective effect against neurotoxicity has been investigated. Material and methods: The primary neuron culture obtained from neonatal rats was exposed to toxicity with paclitaxel and cisplatin and the effect of agmatine on both acute (1 h) and chronic (24 h) exposure was demonstrated by biochemical and molecular analyses. It was demonstrated that the effect of agmatine before and after agmatine was induced by neurotoxicity before agmatine and the effect of agmatine on the formed and occuring toxicities. In addition to the results of cell viability assay, total oxidant capacity and total antioxidant capacity, we have found the opportunity to elaborate on our molecular mechanisms by elaborating our findings with apoptotic and inflammation markers such as caspase 3, kaspase 9 and TNF alpha. Key findings: The results of our study revealed the effect profile of a protective molecule against pathological neural deaths due to neurodegeneration not only in neurotoxicity due to anticancer drugs. Significance: In this context, we tried to reverse neurotoxicity due to anticancer drugs by using agmatine the duration (1 and 24 h) and dosage (10-5M and 10-6 M) determined.Publication Metadata only Antipsychotics: Neurobiological Bases for a Therapeutic Approach(KURE ILETISIM GRUBU A S, 2013) ARICIOĞLU, FEYZA; Gumru, Salih; Aricioglu, FeyzaStudies on the pathophysiology of schizophrenia have become an adventure. It started with a simple pathological approach, focusing only on positive symptoms caused by dopaminergic hyperactivity in mesolimbic system and then branched out with contributions of many different components, including many receptors, various intracellular signaling pathways and gene-environment interactions. These new approaches have been useful in treating the negative symptoms and cognitive impairment observed in schizophrenia. Since there is a bulk of information on the mechanisms causing the disease, a proportional increase in the number of possible new treatment options has been proposed.The most challenging approaches in the disease mechanism address the glutamatergic system, neuroinflammation, neuroplasticity and neurotrophic factors, genetic factors and some intracellular signaling pathways. In this review, all of the above listed factors are discussed in detail.Publication Open Access Future Directions of Cytokine Hypothesis in Depression: 'NLRP3 inflamazomu'(KURE ILETISIM GRUBU A S, 2013-09) ARICIOĞLU, FEYZA; Sahin, Ceren; Ancioglu, FeyzaThe prevalence of depression has been shown to be increased with the presence of chronic inflammatory and/or autoimmune diseases such as rheumatoid arthritis, systemic lupus erythematosus, type II diabetes mellitus and cardiovascular diseases. It has been well documented in the last decade that inflammation in the periphery could interact within the central nervous system. Once an inflammatory stimulus reaches the brain, microglial cells serve as fundamental sensory complements by playing an important role in neuroinflammation which is a necessary process required for brain development. However, the process itself, if excessive or prolonged, can turn into a pathological condition and become a causative factor of the disease, for example, in the case of chronic stress or depression. The association between high plasma levels of pro-inflammatory cytokines and depression has been shown by several clinical and experimental studies. In addition, current antidepressant therapies reduce high cytokine levels of depressive patients and antidepressant-like effects are observed with the use of immunosuppressant drugs acting on cytokine-mediated mechanisms. On the other hand, inflammatory cytokines are known to mediate the activity of the hypothalamic-pituitary axis (HPA) which is well known to be elevated in depression and stress, resulting in a further contribution to the inflammatory state. At present, approximately of patients with depression do not respond to current antidepressant therapies. Thus, great efforts have been made in many studies to provide novel therapeutic approaches for depression. At this point, targeting initiator molecular mechanisms of cytokine-mediated inflammatory responses has become an intriguing approach for preventing the process before the production and release of these inflammatory mediators. Herein, we have aimed to draw attention to a novel aspect of the cytokine hypothesis of depression that may serve as a novel target mechanism and provide further understanding of the disease, namely NLRP3 inflammasome, a multi protein complex formed in macrophage and microglia cells which is responsible for initiating the inflammatory responses mediated with IL-1 beta and IL-18.Publication Open Access Agmatine attenuates stress- and lipopolysaccharide-induced fever in rats(PERGAMON-ELSEVIER SCIENCE LTD, 2005-06) ARICIOĞLU, FEYZA; Aricioglu, F; Regunathan, SPhysiological stress evokes a number of responses, including a rise in body temperature, which has been suggested to be the result of an elevation in the thermoregulatory set point. This response seems to share similar mechanisms with infectious fever. The aim of the present study was to investigate the effect of agmatine on different models of stressors [(restraint and lipopolysaccaride (LPS)] on body temperature. Rats were either restrained for 4 h or injected with LPS, both of these stressors caused an increase in body temperature. While agmatine itself had no effect on body temperature, treatment with agmatine (20, 40, 80 mg/kg intraperitoneally) dose dependently inhibited stress- and LPS-induced hyperthermia. When agmatine (80 mg/kg) was administered 30 min later than LPS (500 mu g/kg) it also inhibited LPS-induced hyperthermia although the effect became significant only at later time points and lower maximal response compared to simultaneous administration. To determine if the decrease in body temperature is associated with an anti-inflammatory effect of agmatine, the nitrite/nitrate levels in plasma was measured. Agmatine treatment inhibited LPS-induced production of nitrates dose dependently. As an endogenous molecule, agmatine has the capacity to inhibit stress- and LPS-induced increases in body temperature. (c) 2005 Elsevier Inc. All rights reserved.Publication Open Access Role of the nitric oxide-soluble guanylyl cyclase pathway in cognitive deficits in streptozotocin-induced diabetic rats(TAYLOR & FRANCIS LTD, 2019-01-02) ARICIOĞLU, FEYZA; Yazir, Yusufhan; Polat, Selen; Utkan, Tijen; Aricioglu, FeyzaOBJECTIVES: The impairment of cognitive functions in diabetes mellitus (DM) is well known. Nitric oxide (NO)-guanyly cyclase (GC)-cyclic guanosine monophosphate (cGMP) pathway is an important role in cognitive functions, and, consequently, phosphodiesterase-5 (PDE-5) inhibitors as well as NO-GC activators are of considerable interest in the treatment of cognitive deficits. Therefore, we aimed to investigate the effects of YC-1 (3-5-hydroxymethyl-2-furyl)-1-benzyl-indazole), an NO-GC activator, and zaprinast, a PDE-5 inhibitor, on cognitive dysfunction in streptozotocin (STZ)-induced diabetic rats. METHODS: Male Wistar rats were divided into five groups (nine rats in each): Control, Vehicle (DMSO), Diabetic (50 mg/kg/i.p. streptozotocin), Diabetic-YC-1 (1 mg/kg/day/i.p., for 4 weeks), and Diabetic-Zaprinast (10 mg/kg/day/i.p., for 4 weeks) group. The Morris water maze, passive avoidance, locomotor activity, and foot shock sensitivity tests were applied to assess the effect of YC-1 and zaprinast on learning and memory. To explore the mechanisms of YC-1 and zaprinast on learning and memory performance, protein expressions of brain-derived neurotrophic factor (BDNF) in hippocampus were examined immunohistochemically. RESULTS: Thirty days after the induction of DM, rats exhibited severe learning and memory dysfunctions associated with decreased BDNF expression. Both chronic YC-1 and zaprinast treatment improved cognitive performance and hippocampal BDNF expression in diabetic rats. In the locomotor activity and foot shock sensitivity test, no significant differences were observed between the groups. Furthermore, hyperglycaemia did not affect cognition enhancement effects of YC-1 or zaprinast in diabetic rats. CONCLUSIONS: Our findings highlight the beneficial effects of nitric oxide-guanylyl cyclase activators and PDE-5 inhibitors to improve cognitive function in diabetes.Publication Open Access Agmatine, A Metabolite of Arginine, Improves Learning and Memory in Streptozotocin-Induced Alzheimer's Disease Model in Rats(KURE ILETISIM GRUBU A S, 2016-12) ARICIOĞLU, FEYZA; Sirvanci-Yalabik, Muge; Sehirli, Ahmet Ozer; Utkan, Tijen; Aricioglu, FeyzaObjective: Agmatine, the decarboxylation product of arginine produced by arginine decarboxylase, is a novel neurotransmitter and exists in the mammalian brain. Agmatine has been reported to modulate cognitive functions, including learning and memory. Methods: In the present study, we evaluated the effects of agmatine on cognitive performance and oxidative damage in intracerebroventricular (i.c.v.) streptozotocin (STZ) model of Alzheimer's disease (AD). Adult male Sprague-Dawley rats were injected STZ (3mg/kg, i.c.v, bilaterally) on days 1 and 3. The learning and memory patterns were assessed by using passive avoidance, Morris water maze, and closed field activity tests. Also, malondialdehyde (MDA), glutathione (GSH) levels and myeloperoxidase (MPO) activity have been determined as the parameters of oxidative damage. The behavioral tests were performed after 14 days from the first injection of STZ. Rats with impaired learning and memory performance were treated with intraperitoneal (i.p.) agmatine (40 mg/kg) twice daily for 7 days. After agmatine treatment, rats were subjected to the aforementioned behavioral tests again. Immediately after decapitation of the rats, the brains were collected and analyzed for oxidative damage parameters. Results: Agmatine improved the STZ-induced both spatial and emotinal memory impairment and oxidative damage. Findings of the study demonstrated the effectiveness of agmatine in reversing the cognitive deficits as well as the oxidative damage caused by i.c.v STZ. Conclusion: Taken together, our results have provided experimental evidence suggesting a possible therapeutic potential of agmatine as a regulator in etiopathogenesis of neurodegenerative diseases such as Alzheimer's disease.Publication Metadata only Effect of harmane, an endogenous beta-carboline, on learning and memory in rats(PERGAMON-ELSEVIER SCIENCE LTD, 2013) ARICIOĞLU, FEYZA; Celikyurt, Ipek Komsuoglu; Utkan, Tijen; Gocmez, Semil Selcen; Hudson, Alan; Aricioglu, FeyzaOur aim was to investigate the effects of acute harmane administration upon learning and memory performance of rats using the three-panel runway paradigm and passive avoidance test. Male rats received harmane (2.5, 5, and 7.5 mg/kg, i.p.) or saline 30 min. before each session of experiments. In the three panel runway paradigm, harmane did not affect the number of errors and latency in reference memory. The effect of harmane on the errors of working memory was significantly higher following the doses of 5 mg/kg and 7.5 mg/kg. The latency was changed significantly at only 7.5 mg/kg in comparison to control group. Animals were given pre-training injection of harmane in the passive avoidance test in order to determine the learning function. Harmane treatment decreased the retention latency significantly and dose dependently, which indicates an impairment in learning. In this study, harmane impaired working memory in three panel runway test and learning in passive avoidance test. As an endogenous bioactive molecule, harmane might have a critical role in the modulation of learning and memory functions. (c) 2012 Elsevier Inc. All rights reserved.Publication Metadata only Glycogen Synthase Kinase-3: A New Therapeutic Target in Mood Disorders(KURE ILETISIM GRUBU A S, 2013) ARICIOĞLU, FEYZA; Aricioglu, Feyza; Gumru, SalihMood disorders, including major depressive disorder and bipolar disorder, are common and largely inadequately treated. Additionally, little is known about their etiologies. Glycogen synthase kinase-3 (GSK-3) is a serine/threonine protein kinase, interacting with many signaling pathways. In 1996, lithium was found to inhibit GSK-3 and this discovery led us to the possibility that impaired GSK-3 inhibition is related with mood disorders. In time, animal and human studies encouraged this finding. Evidence is reviewed that depression may be associated with impaired inhibitory control of GSK-3, and mania with hyperstimulation of GSK-3. Mood disorders may result in part from impairments in mechanisms controlling the activity of GSK-3 or GSK-3-regulated functions and substantial evidence supports the conclusion that bolstering the modulatory control of GSK-3 is an important component of the therapeutic actions of drugs used to treat mood disorders and that GSK-3 is a valid target for developing new therapeutic interventions. Future research should identify the causes of dysregulation of GSK-3 in mood disorders and the actions of GSK-3 that contribute to these diseases.