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 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 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 Open 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 ZaferObjective: 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.Publication Open 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.].Publication Metadata only Studies on the role of alpha 7 nicotinic acetylcholine receptors in K562 cell proliferation and signaling(SPRINGER, 2021) AYDIN OMAY, BANU; Narin, Gozde Onder; Aydin, Banu; Cabadak, HulyaThe results we obtained from this study gave information about the determination of alpha 7 nicotinic acetylcholine receptor (alpha 7-nACh) expression in human erythroleukemia cells, as well as whether it has a role in calcium release and cell proliferation in the presence of nicotinic agonist, antagonists. Determining the roles of alpha 7 nicotinic receptors in erythroleukemia cells will also contribute to leukemia-related signal transduction studies. This study is primarily to determine the role of nicotinic agonists and antagonists in cell proliferation, alpha 7 nicotinic acetylcholine receptor expression, and calcium release. The aim of this study, which is a continuation and an important part of our previous studies on the cholinergic system, has contributed to the literature on the human erythroleukemia cell signaling mechanism. Cell viability was evaluated by the trypan blue exclusion test and Bromodeoxyuridine/5-Bromo-2 '-deoxyuridine (BrdU) labeling. Acetylcholine, nicotinic alpha 7 receptor antagonist methyllycaconitine citrate, and cholinergic antagonist atropine were used to determine the role of alpha 7-nACh in K562 cell proliferation. In our experiments, the fluorescence spectrophotometer was used in Ca2+ measurements. The expression of nicotinic alpha 7 receptor was evaluated by western blot. The stimulating effect of acetylcholine in K562 cell proliferation was reversed by both the alpha 7 nicotinic antagonist methyllycaconitine citrate and the cholinergic antagonist, atropine. Methyllycaconitine citrate inhibited K562 cell proliferation partially explained the roles of nicotinic receptors in signal transduction. While ACh caused an increase in intracellular Ca2+, methyllycaconitine citrate decreased intracellular Ca2+ level in K562 cell. The effects of nicotinic agonists and/or antagonists on erythroleukemic cells on proliferation, calcium level contributed to the interaction of nicotinic receptors with different signaling pathways. Proliferation mechanisms in erythroleukemic cells are under the control of the alpha 7 nicotinic acetylcholine receptor via calcium influx and different signalling pathway.Publication Metadata only Cross-Talk of Cholinergic and ?-Adrenergic Receptor Signalling in Chronic Myeloid Leukemia K562 Cells(2022) AYDIN OMAY, BANU; Aydın, Banu; Gören, Mehmet Zafer; Kanlı, Zehra; Cabadak, HülyaPublication Metadata only Hepatosellüler karsinomada glut1 inhibitörü bay-876’nın hepg2 hücrelerinde ve steatoz hücre modelinde glukoz alımı ve hücre çoğalmasına etkisi(2022-12-09) AYDIN OMAY, BANU; CABADAK, HÜLYA; Tanriverdi Bademci A. M., Aydın Omay B., Cabadak H.Hepatocellular carcinoma is one of the deadly cancers with a significant incidence worldwide. In cancer cells, aerobic glycolysis increases with the Warburg effect. Glucose transport across the cell membrane becomes important at this stage. It has been found that there is an increase in GLUT1 expression in various cancers. BAY-876 is a new generation GLUT1 inhibitor. The affinity of BAY-876 for GLUT1 was found to be approximately 100 times higher than for other glucose transporters. HepG2 cells will be used in molecular analyzes to investigate the role of this novel GLUT1 inhibitor in GLUT1-mediated cell proliferation and glucose uptake into the cell.The effect of BAY-876 on glucose uptake was investigated in the case of bioenergetic stress by applying metformin, an insulin-sensitizing agent with strong antihyperglycemic properties, and in hypoxic environment by applying CoCl2 treatment. A steatosis cell model was created using oleic acid and palmitic acid. We aimed to investigate the effects of BAY-876 on cell proliferation and glucose uptake in HepG2 cell line and HepG2 steatosis cell model. Drugs were added to the culture medium. its effect on cell proliferation was investigated with the BrDU method. Cell proliferation, glucose uptake and colony formation were investigated in HepG2 cell line and HepG2 steatosis cell model in the presence and absence of BAY-876. BAY-876 inhibits cell proliferation and reduces glucose uptake in HepG2 cells and steatosis cell model. BAY-876 was also found to reduce glucose uptake in normal and steatosis cell models under bioenergetic and hypoxic stress conditions. It is predicted that our study will contribute to the literature, provide a different perspective to anticancer drug research studies of GLUT1 inhibitor and contribute to the elucidation of the signal transmission mechanism of hepatocellular carcinoma.