Person: AYDIN OMAY, BANU
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AYDIN OMAY
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Publication Metadata only The effect of metformin on ethanol- and indomethacininduced gastric ulcers in rats(2022-09-01) YÜKSEL, MERAL; ERCAN, FERİHA; CABADAK, HÜLYA; AYDIN OMAY, BANU; İpek B. E. , YÜKSEL M., Cumbul A., ERCAN F., CABADAK H., AYDIN OMAY B., Alican İ.BACKGROUND: Previous studies found metformin as an effective agent to suppress oxidative stress, inflammation, and apoptosis in various inflammatory diseases. The present study investigated the effect of metformin against 2 experimental gastric injury models in rats, using macroscopical, histopathological, biochemical, and immunostaining studies. METHODS: After 24 hours of fasting, male Sprague-Dawley rats (280-400 g) (n = 8 per group) received indomethacin (80 mg/kg; indo ulcer group) or absolute ethanol (5 mL/kg; ethanol ulcer group) or vehicle orally by gavage. Metformin (500 mg/kg) was given orally for 3 days prior to indomethacin or ethanol challenge. Ranitidine (50 mg/kg) was given orally for 3 days before indomethacin or ethanol administration as a positive control. On day 3, the animals were euthanized 6 hours after indo or 1 hour after ethanol challenge. Gastric samples were used for macroscopic scoring, histopathological examinations, and biochemical assays. Trunk blood was collected for the assessment of interleukin-1β level. RESULTS: In both ethanol ulcer and indo ulcer groups, metformin decreased the extent of gastric lesions macroscopically and microscopically, improved the high chemiluminescence levels, and the percentage of terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL)-positive apoptotic cells compared with untreated ulcer groups. Gastric blood flow analysis revealed significant increases in both metformin-treated ulcer groups compared to untreated ulcer groups. CONCLUSION: The findings of the present work demonstrated the gastroprotective effect of metformin against the development of gastric mucosal lesions induced by ethanol and indomethacin in non-diabetic, normoglycemic rats via its antioxidant and anti-apoptotic properties and partly from its ability to restore blood flow.Publication Metadata only Atipamezole, a specific alpha(2A) antagonist, suppresses spike-and-wave discharges and alters Ca2+/calmodulin-dependent protein kinase II in the thalamus of genetic absence epilepsy rats(WILEY, 2020) AYDIN OMAY, BANU; Yavuz, Melis; Aydin, Banu; Carcak, Nihan; Akman, Ozlem; Raci Yananli, Hasan; Onat, FilizObjective The role of alpha(2A) adrenergic receptors (alpha(2A)ARs) in absence epilepsy is not well characterized. Therefore, we investigated the outcomes of the specific antagonism of alpha(2A)ARs on the spike-and-wave discharges (SWDs) in genetic absence epilepsy rats from Strasbourg (GAERSs), together with its influence on the behavior and second messenger systems, which may point to the mechanisms to which a possible SWD modulation can be related. Methods Atipamezole, an alpha(2A)AR antagonist, was administered intracerebroventricularly to the adult GAERSs, and electroencephalography (EEG) was conducted. The cumulative duration and number of SWDs, and the mean duration of each SWD complex were counted. The relative power of the EEG frequency bands and behavioral activity after the acute application of two doses (12 and 31 mu g/5 mu L) of atipamezole were evaluated. The levels of cyclic adenosine monophosphate and calcium/calmodulin-dependent kinase II (CaMKII) were measured in the cortex, thalamus, and hippocampus of naive Wistar rats and GAERSs, administered with artificial cerebrospinal fluid (aCSF) as a vehicle, or either acute or chronic atipamezole (12 mu g), the latter being administered for 5 consecutive days. Results Atipamezole significantly suppressed SWDs dose-dependently, without affecting the relative power values of EEG frequency spectrum. The stereotypic activity was significantly lower in both naive Wistar rats and GAERSs receiving the highest dose (31 mu g) of atipamezole compared to GAERSs receiving aCSF. In GAERSs, CaMKII levels were found to be higher in the thalamus after the acute and chronic application of SWD-suppressing doses of atipamezole (12 and 31 mu g) compared to aCSF. Significance This study emphasizes the alpha(2)AR-related modulation of absence epilepsy and particularly the significance of alpha(2)AR antagonism in suppressing SWDs. Atipamezole's SWD-suppressive actions may be through CaMKII-mediated second messenger systems in the thalamus.Publication Metadata only Decreased Hyperpolarization-Activated Cyclic Nucleotide-Gated Channel 2 Activity in a Rat Model of Absence Epilepsy and the Effect of ZD7288, an Ih Inhibitor, on the Spike-and-Wave Discharges(KARGER, 2022) AYDIN OMAY, BANU; Yavuz, Melis; Aydin, Banu; Carcak, Nihan; Onat, FilizIntroduction: Hyperpolarization-activated cyclic nucleotide-gated (HCN) channel currents of Ih and absence epilepsy seizures are associated, but studies reveal differential results. Objective: In our study, we aimed to investigate the role of the HCN channels on the expression of spike-and-wave discharges (SWDs) using the Genetic Absence Epilepsy Rats from Strasbourg (GAERS) model. Methods: HCN isoform levels from isolated brains of both naive nonepileptic Wistar and GAERS groups were evaluated by enzyme-linked immunosorbent assay. ZD7288, an Ih inhibitor as well as an HCN channel antagonist, was administered intracerebroventricularly to the adult GAERS groups, and to evaluate their SWD activities, electroencephalography was recorded. The effect of ZD7288 on the cumulative total duration and number of SWDs and the mean duration of each SWD complex was evaluated. Results: The HCN2 levels in the cortex and hippocampus of the GAERS group were lower compared to the naive nonepileptic Wistar group (p < 0.05). ZD7288 increased the number of SWDs at the 20th and 120th min with the highest administered dose of 7 mu g (p < 0.05). Conclusion: The Ih inhibitor ZD7288 increased the number of SWDs in a genetic absence epilepsy rat model, although this increase may not be significant due to the inconsistent time-dependent effects. In GAERS, the cortical and hippocampal HCN2 channel levels were significantly lower compared to the control group. Further studies are needed with higher doses of ZD7288 to determine if the effects will increase drastically.Publication Metadata only Role of cholinergic agents in proliferation and caspase activity of hemin-induced erythroid differentiated K562 cells(TAYLOR & FRANCIS LTD, 2020) AYDIN OMAY, BANU; Cabadak, Hulya; Aydin, BanuBackground: Muscarinic receptors have many functions in the cells and tissues. Acetylcholine (ACh) plays an important role in cellular physiology. ACh also acts at the different parts of the central nervous system and nonneuronal cells. Cholinergic receptors also have different functions in many cell types and tissues. Caspases (cysteine aspartic proteases and cysteine aspartases) are cysteine dependent aspartate-specific proteases. They are an important role in necrosis and cell death and inflammation signaling pathways. They are also the primary mediators of apoptosis. During apoptosis, different caspase types participate in different functions. We have previously shown that carbachol (CCh) inhibits K562 cell proliferation. This study was performed to investigate the anti-tumor efficacy of cholinergic drugs in hemin-induced erythroid differentiated K562 cells. The aim of this study was to address the mechanism of cholinergic drugs on hemin-induced erythroid differentiated K562 cell proliferation and caspase activities. We detected M-3 muscarinic receptor expression in erythroid differentiated K562 cell line. Methods: K562 cells were differentiated with hemin (50 mu M). The expression of the M-3 muscarinic receptor was detected by the western blotting technique. Erythroid differentiated K562 cells treated with CCh (100 mu M). After 24 and 48 h, cells were counted by BrdU cell proliferation kit. Caspase 3,8, and 9 activities were measured by enzyme-linked immunosorbent assay (ELISA) kits according to the manufacturer's instructions. Results: Erythroid differentiated K562 cell proliferation was not significantly increased after CCh treatment. In the meantime, caspases 8 and 9 activities in erythroid differentiated K562 cell line was significantly higher than undifferentiated K562 cells (p < .05).Publication Metadata only Contribution of M-1 and M-2 muscarinic receptor subtypes to convulsions in fasted mice treated with scopolamine and given food(ELSEVIER SCIENCE BV, 2019) AYDIN OMAY, BANU; Bacanak, Merve Saygi; Aydin, Banu; Cabadak, Hulya; Nurten, Asiye; Goren, Mehmet Zafer; Enginar, NurhanTreatment of fasted mice and rats with the nonselective muscarinic antagonist, scopolamine or atropine, causes convulsions after food intake. This study evaluated the effect of fasting on the expression of M-1 and M-2 muscarinic receptors in the brain regions, the relationship between receptor expression and seizure stages, and the muscarinic receptor subtype which plays a role in the occurrence of convulsions. Mice were grouped as allowed to eat ad lib (fed) and deprived of food for 24 h (fasted). Fasted animals developed convulsions after being treated with scopolamine (60%) or the selective M-1 receptor antagonist pirenzepine (10 mg/kg; 20% and 60 mg/kg; 70%) and given food. Fasting increased expression of M-1 receptors in the frontal cortex and M-2 receptors in the hippocampus, but produced no change in the expression of both receptors in the amygdaloid complex. Food intake after fasting decreased M-1 receptor expression in the frontal cortex and M-1 and M-2 receptor expression in the hippocampus. Seizure severity was uncorrelated with muscarinic receptor expression in the brain regions. Taken together, these findings provide evidence for the role of M-1 muscarinic receptor antagonism and fasting-induced increases in M-1 and M-2 expression possible underlying mechanism in the occurrence of convulsions in fasted animals.Publication Metadata only Flavonoid ile Kombine Edilmiş Kemoterapi İlaçlarının Kolorektal Kanser Hücrelerine Etkisi(2022-12-09) AYDIN OMAY, BANU; ERZİK, CAN; ARĞA, KAZIM YALÇIN; CABADAK, HÜLYA; Kanlı Z., Aydın Omay B., Erzik C., Arğa K. Y. , Cabadak H.Publication Metadata only Muscarinic receptor-mediated nitric oxide release in a K562 erythroleukaemia cell line(2009) AYDIN OMAY, BANU; Cabadak H., Küçükibrahimoǧlu E., Aydin B., Kan B., Gören M.Z.1 In the present study we have investigated the expression of muscarinic receptors in K562 erythroleukaemic cells and the effects of muscarinic agonist and antagonists on extracellular citrulline levels in these cells, as a marker of nitric oxide (NO) generation. 2 Muscarinic acetylcholine receptors (M 1-M5) play key roles in regulating many diverse physiological processes. Recent studies suggest that muscarinic receptors mediate some cellular events in haematopoietic cells. Multiple subtypes of muscarinic receptors are expressed in different human cells. NO, a free radical and a signaling molecule, is involved in the regulation of many physiological functions and derived from certain nitric oxide synthases (NOS), which are related to muscarinic receptors. 3 In this study, the presence of M2, M3 and M4 subtypes in K562, an erythroleukaemic cell line, was demonstrated by using the reverse transcriptase-polymerase chain reaction. Moreover, the generation of NO induced by carbachol, a non-selective muscarinic agonist, was investigated by using high-performance liquid chromatography to measure changes in extracellular l-citrulline levels. 4 We found that carbachol enhanced l-citrulline production in K562 erythroleukaemic cells. The effect of carbachol on l-citrulline production was antagonized by atropine and 4-diphenylacetoxy-N-methylpiperidine (4-DAMP), while tropicamide had little effect. These results suggest that the muscarinic receptor M 3 subtype may mediate NO signaling in K562 erythroleukaemic cells. © 2009 Blackwell Publishing Ltd.Publication Metadata only The role of intracellular pathways in the proliferation of human K562 cells mediated by muscarinic receptors(PERGAMON-ELSEVIER SCIENCE LTD, 2013) AYDIN OMAY, BANU; Aydin, Banu; Kan, Beki; Cabadak, HulyaMuscarinic acetylcholine receptors (mAChRs) are members of the superfamily of G protein coupled receptors (GPCRs). Muscarinic receptors are relatively abundant in the central nervous system and in the peripheral parasympathetic nervous system. Several studies have suggested that muscarinic receptors also mediate some cellular events in hematopoietic cells. K562 erythroleukemia cells contain muscarinic receptors M-2, M-3 and M-4, and activation of muscarinic receptors changes cell proliferation. We examined the effects of several compounds on cell proliferation in K562 erythroleukemia cells. These included a muscarinic receptor agonist carbachol (CCh), a protein kinase inhibitor staurosporine; the phospholipase C inhibitor U73122, the MEK 1-2 inhibitor UO126, the PI3-kinase inhibitor wortmannin, the Ca2+ chelators BAPTA/AM and 2-aminoethoxy-diphenylborate (2APB). In addition, we also investigated muscarinic receptor mediated protein kinase C (PKC) expression in K562 cells. CCh caused a decrease in DNA synthesis in K562 cells supplemented with 1% fetal bovine serum after starvation. Pre-treatment of K562 cells with U73122 and BAPTA/AM antagonized the inhibitory effect of CCh, suggesting that phospholipase C and intracellular calcium are involved in CCh-mediated inhibition of proliferation in K562 cells. Our data also suggest that the regulatory roles of protein kinase C and the MAPK/ERK pathways in K562 cell proliferation are independent of cholinergic activation. (C) 2013 Elsevier Ltd. All rights reserved.Publication Metadata only Increased Noradrenaline Levels in the Rostral Pons can be Reversed by M1 Antagonist in a Rat Model of Post-traumatic Stress Disorder(SPRINGER/PLENUM PUBLISHERS, 2013) AYDIN OMAY, BANU; Terzioglu, Berna; Kaleli, Melisa; Aydin, Banu; Ketenci, Sema; Cabadak, Hulya; Goren, M. ZaferThe dysregulation of hypothalamic-pituitary-adrenal axis and noradrenergic, serotonergic and glutamatergic systems are thought to be involved in the pathophysiology of post-traumatic stress disorder. The effect of selective M1 muscarinic receptor antagonist, pirenzepine on anxiety indices was investigated by using elevated plus maze, following exposure to trauma reminder. Upon receiving the approval of ethics committee, Sprague-Dawley rats were exposed to dirty cat litter (trauma) for 10 min and 1 week later, the rats confronted to a trauma reminder (clean litter). The rats also received intraperitoneal pirenzepine (1 or 2 mg/kg/day) or saline for 8 days. Noradrenaline (NA) concentration in the rostral pons was analyzed by HPLC with electrochemical detection. The anxiety indices of the rats subjected to the trauma reminder were increased when compared to control rats (p < 0.05). Pirenzepine treatment in traumatized rats displayed similar anxiety indices of non-traumatized rats treated with physiological saline. Although freezing time was prolonged with pirenzepine in traumatized groups the change was not found statistically significant. The NA level was 1.5 +/- A 0.1 pg/mg in non-traumatized rats and increased to 2.4 +/- A 0.2 pg/mg in traumatized rats. Bonferroni post hoc test revealed that the NA content of the rostral pons of the traumatized rats treated with physiological saline was significantly higher than the content of other groups (p < 0.01). We conclude that NA content in the rostral pons increases in respect to confrontation to a trauma reminder which can be reversed by M1 antagonist pirenzepine indicating the roles of M1 receptors.Publication Metadata only Effects of melatonin supplementation and different exercise models on cognitive function in long-term exposure to constant light in rats(2023-01-01) YILDIRIM, HATİCE SELİN; AYDIN OMAY, BANU; KASIMAY ÇAKIR, ÖZGÜR; Erol G., Dincer B. E., Calik H. N., Oksuz H., YILDIRIM H. S., Sener D., AYDIN OMAY B., KASIMAY Ö.