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ARICIOĞLU, FEYZA

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ARICIOĞLU

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FEYZA

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Open Access
Inhibition of Neuronal Nitric Oxide Synthase and Soluble Guanylate Cyclase Prevents Depression-Like Behaviour in Rats Exposed to Chronic Unpredictable Mild Stress
(WILEY, 2012-03) ARICIOĞLU, FEYZA; Yazir, Yusufhan; Utkan, Tijen; Aricioglu, Feyza
Depression is the most common psychiatric disorder. It is well established that endogenous nitric oxide (NO) contributes to chronic unpredictable mild stress (CUMS)-induced depression. The aim of this study was to investigate brain-derived neurotropic factor (BDNF) expression in CUMS-induced depression-like behaviour in rats. Rats were exposed to CUMS for 5 weeks. A specific and selective nNOS inhibitor, 3-bromo-7-nitroindazole (3-Br-7-NI; 20 mg/kg/day, i.p.), and a specific soluble guanylate cyclase (sGC) inhibitor, 1H-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-one (ODQ; 10 mg/kg/day, i.p.), were administered during CUMS. The forced swimming test (FST) was used to assess despair and sucrose consumption, and sucrose preference test was used to assess anhedonia that are the main symptoms of the depression. We show that both 3-Br-7-NI and ODQ administration during CUMS suppressed CUMS-induced, depression-like behavioural changes, including reduced sucrose preference, body-weight and locomotor activity as well as increased immobility time in the FST. CUMS also significantly decreased BDNF protein levels in the CA1 and CA3 regions of the hippocampus, which was reversed by 3-Br-7-NI and ODQ administration. Our findings suggest a novel role for nNOS and sGC-cGMP in the development of the CUMS model of depression.
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, Norbert
Schizophrenia 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.
Open Access
Effects of agmatine on cognitive functions during vascular dementia in biological aging through eNOS and BDNF expression
(TAYLOR & FRANCIS LTD, 2017-04-03) ARICIOĞLU, FEYZA; Bagci, Bulent; Utkan, Tijen; Yazir, Yusufhan; Aricioglu, Feyza; Ozturk, Gokce Sevim; Sarioglu, Yusuf
Objective: Biological aging has been recognized to cause impairment of memory and the development of vascular dementia. Based on our previous work, agmatine has been shown to have a beneficial effect and might have therapeutic potential on cognitive functions, including learning and memory. The aim of the present study was to examine the possible effect of agmatine on biological aging-induced vascular endothelial dysfunction and associated dementia in rats. Methods: We used three different age groups (4-month-olds, 18-month-olds and 24-montholds; n = 12 in each group) of control and agmatine-treated rats. Control animals received physiological saline for 8 weeks. Agmatine sulfate (40 mg/kg, twice daily) was given to the agmatine groups orally for 8 weeks. Herein, we investigated the effects of agmatine on systolic blood pressure (SBP), nitric oxide (NO)-mediated endothelium-dependent and - independent vasorelaxant responses in thoracic aorta, cognitive performance (passive avoidance test; PAT, and Morris water maze test; MWMT), endothelial nitric oxide synthase (eNOS) expression and both hippocampal and amygdaloid brain-derived neurotrophic factor (BDNF) expression in aged rats. Results: We found cognitive decline, endothelial dysfunction and reduced eNOS and BDNF expression in aged rats. All these changes may result from aging-induced vascular dementia. We also found that chronic treatment with agmatine may improve amygdala-dependent emotional and spatial learning and memorial performance, and endothelial function, and may regulate eNOS and BDNF protein expression in aged rats. Conclusion: Results of the current study point out that chronic agmatine treatment may prevent endothelial dysfunction associated with vascular dementia through eNOS and BDNF expression in aged rats.
Open Access
Comparison of behavioural and molecular effects of two different schizophrenia models induced by subchronic MK-801 administration in rats
(MARMARA UNIV, FAC PHARMACY, 2018-04-06) ARICIOĞLU, FEYZA; Unal, Gokhan; Aricioglu, Feyza
Schizophrenia is a severe psychiatric disorder with about 1% prevalance. NMDA receptor antagonists such as Phencyclidine (PCP) and MK-801 are commonly used for modeling schizophrenia in rodents. In literature, despite of the concensus about subchronic PCP administration (commonly 7 days, bi-daily administration followed by a 1 week washout period), there are different subchronic administration regimens for MK-801 beside 7 days, bidaily (MK-801-7), such as 14 days (MK-801-14) daily or 28 days daily injections. In this study, we aimed to compare two prevalant MK-801 models (MK-801-7 and MK-801-14, 0.2 mg/kg)in both behavioural and molecular changes. Wistar Hannover rats grouped as control (n=10), MK-801-14 (n=8) and MK-801-7 (n=8). Prepulse inhibition of acustic startle response (PPI), novel object recognition test (NORT), social interaction (SI) and Morris's water maze (MWM) tests were used for behavioural analyzes while real time polimerase chain reaction (Rt-PCR) was conducted for molecular analyzes of glutamic acid decarboxilase 67 (GAD67) and parvalbumin. Our results showed decreased PPI in MK-801-14 and MK-801-7 groups. Moreover, in both models platform finding latencies were increased and swimming time in platform area was decreased in MWM. MK-801-14 and MK-801-7 reduced following and raised avoiding behaviours in SI. In Rt-PCR, GAD67 mRNA levels were decreased by MK-801-14 and MK-801-7 administrations. However, only MK-801-7 decreased discrimination index in NORT and parvalbumin mRNA levels. In this study, it has been showed that although MK-801-14 and MK-801-7 administrations revealed smiliar schizophrenia like symptoms in rats, MK-801-7 has partial superiories in certain aspects.
Open Access
Synthesis and anticonvulsant activity of some 2-pyrazolines derived from chalcones
(ELSEVIER SCIENCE BV, 2017-05) KAYMAKÇIOĞLU, BEDİA; Beyhan, Nagihan; Kocyigit-Kaymakcioglu, Bedia; Gumru, Salih; Aricioglu, Feyza
Synthesis of chalcones (1,3-diarylprop-2-en-1-ones) and 2-pyrazoline derivatives has been an active field of research due to their established pharmacological effects. In this study, a series of chalcones were prepared with methyl aryl ketones and substituted aldehydes in the presence of sodium hydroxide and methanol through Claisen-Schmidt condensation. 3,5-Disubstituted4,5-dihydro-1H-pyrazole-1-carbothioamides were synthesized by refluxing selected chalcones and thiosemicarbazide in alkaline medium. Similarly N-3,5-trisubstituted-4,5-dihydro-1H-pyrazole-1-carboxamides were synthesized by refluxing selected chalcones with N-(4-chlorophenyl) semicarbazide in alkaline medium. Structures of the synthesized compounds were confirmed by elemental analysis and spectral (UV, IR, H-1 NMR, C-13 NMR, and mass) data, which were in line with the proposed structures. All compounds were tested for their anticonvulsant activity using pentylenetetrazole induced seizure (PTZ) and maximal electroshock seizure (MES) tests in mice at a dose level of 50 mg/kg. Among the 2-pyrazoline-1-carbothioamide derivatives, 5-(2,6-dichlorophenyl)-3-(thiophen-2-yl)-4,5-dihydro-1H-pyrazole-1-carbothioamide (2e) reduced grade-5 seizure activity and also increased survival rate in PTZ test. In MES test, 5-(4-methoxyphenyl)-3-[4-(methylsulphonyl) phenyl]-4,5-dihydro-1H-pyrazole-1-carbothioamide(2g) has not only decreased seizure severity, but also increased survival rate. Among the 2-pyrazoline-1-carboxamide derivatives, 3-(5-bromothiophen-2-yl)-N-(4-chlorophenyl)-5-(2,6-dichlorophenyl)-4,5-dihydro-1H-pyrazole-1-carboxamide (3d) having 5-bromothiophen and 2,6-dichlorophenyl moieties and N-(4-chlorophenyl)-5-(2,6-dichloro-phenyl)-3-(5-chlorothiophen-2-yl)-4,5-dihydro-1H-pyrazole-1-carboxamide (3e) having 5-chlorothiophen and 2,6-dichlorophenyl moieties showed remarkable activities in PTZ test. Among all tested derivatives, compound 3d was found to be the most active one and reduced grade-5 seizure severity and also increased survival rate. (C) 2013 Production and hosting by Elsevier B.V. on behalf of King Saud University.
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, S
Agmatine 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.
Open Access
Antidepressant-like Effects Induced by Chronic Blockade of the Purinergic 2X7 Receptor through Inhibition of Non-like Receptor Protein 1 Inflammasome in Chronic Unpredictable Mild Stress Model of Depression in Rats
(KOREAN COLL NEUROPSYCHOPHARMACOLOGY, 2019-05-31) ARICIOĞLU, FEYZA; Aricioglu, Feyza; Ozkartal, Ceren Sahin; Bastaskin, Tugce; Tuzun, Erdem; Kandemir, Cansu; Sirvanci, Serap; Kucukali, Cem Ismail; Utkan, Tijen
Objective: Purinergic 2X7 receptor (P2X7R) activation is known to be involved in pathogenesis of depression. Our aims were to investigate P2X7R-activated inflammasome pathways in parallel with induction of depression and to test the antidepressant-like effects of the selective P2X7R antagonist Brilliant Blue G (BBG) in a rat model of chronic unpredictable mild stress (CUMS). Methods: Male Wistar albino rats were divided into control, CUMS, CUMS+BBG25 (25 mg/kg/day) and CUMS+BBG50 (50 mg/kg/day) groups (n=10 for each group). Various stressors were applied to rats for 6 weeks to establish the CUMS model and daily BBG treatment was started at the end of 3rd week. Sucrose preference test and forced swim test (FST) were performed to assess antidepressant-like effects. Brain samples were obtained for real-time polymerase chain reaction and immunohistochemistry analysis. Results: In FST, duration of immobility was reduced in the CUMS+BBG50 group. Also, BBG treatment significantly enhanced sucrose preference. While NLRP3 gene expression levels were unchanged in rats exposed to the CUMS protocol, expression levels of other inflammasome pathway factors NLRP1, caspase-1, ASC, NF-kappa B, IL-1 beta, IL-6 and P2X7R were increased. BBG treatment reduced expression levels of these factors. Likewise, Iba-1 and GFAP immunoreactivities were enhanced by the CUMS protocol and this action was reversed by BBG treatment. Conclusion: Chronic administration of BBG in CUMS model results in antidepressant-like activity in a dose dependent manner. Molecular and histological results show that these effects might be at least partially related to the suppression of inflammasome-related neuroinflammatory responses and suggest involvement of NLRP1 in depression.
Open Access
Regulation of GSK-3 Activity as A Shared Mechanism in Psychiatric Disorders
(KURE ILETISIM GRUBU A S, 2014-03) ARICIOĞLU, FEYZA; Sahin, Ceren; Unal, Gokhan; Aricioglu, Feyza
Glycogen synthase kinase-3 (GSK-3), a member of the serine/threonine kinase family was first identified as an inhibitor of the metabolic enzyme glycogen synthase and is now accepted as a widely influential enzyme responsible for many intracellular regulatory mechanisms with over 50 known substrates characterized. There are two mammalian GSK-3 isoforms encoded by separate genes: GSK-3 alpha and GSK-3 beta with high structural homology. Both GSK-3 alpha and GSK-3 beta are widely expressed in many tissues with the highest levels in the brain and their functions are generally considered to be indistinguishable. Unlike many other protein kinases, GSK-3 is constitutively dephosphorylated and active in resting cells. Phosphorylation of GSK-3 by other protein kinases such as PKA (Protein kinase A), AKT (Protein kinase B) and PKC (Protein kinase C) inhibits its activity. Today a growing body of evidence strongly suggests that increased GSK-3 activity is involved in the development of schizophrenia and mood disorders such as bipolar disorder, major depression and hyperactivity associated disorders. Thus, inhibition of overactive GSK-3 has become a promising target in the treatment of these psychiatric disorders. Herein we will briefly discuss the underlying mechanisms related to how GSK-3 is thought to participate in such diseases and will give examples of clinically important treatments that have a role in GSK-3 regulation.
Open Access
Future Directions of Cytokine Hypothesis in Depression: 'NLRP3 inflamazomu'
(KURE ILETISIM GRUBU A S, 2013-09) ARICIOĞLU, FEYZA; Sahin, Ceren; Ancioglu, Feyza
The 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.
Open Access
Agmatine attenuates stress- and lipopolysaccharide-induced fever in rats
(PERGAMON-ELSEVIER SCIENCE LTD, 2005-06) ARICIOĞLU, FEYZA; Aricioglu, F; Regunathan, S
Physiological 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.