Person: CABADAK, HÜLYA
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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 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 Open Access The role of Glu N1 activated nitric oxide synthase in rat model of post traumatic stress disorder(2016-01-01) AYDIN OMAY, BANU; CABADAK, HÜLYA; GÖREN, MEHMET ZAFER; ayhan B. G., AYKAÇ A., gür k., AYDIN B., Seçgin E., Seven İ., CABADAK H., GÖREN M. Z.Objectives: Activation of neuronal nitric oxide synthase (nNOS) and interrelated alterations of calmodulin and ionotropic glutamate receptor (GluN1) levels are unknown in post traumatic stress disorder (PTSD). Materials and Methods: Sprague-Dawley rats of both sexes were exposed to to dirty cat litter, and then placed on an elevated plus maze. An anxiety index was calculated and tissue samples from hippocampus and amygdala were prepered in order to to detect calmodulin, NOS and GluN1 by immunoblotting. Results: The anxiety indices of the traumatized rats were markedly higher than those of the controls (p<0.05). GluN1 and calmodulin levels were decreased in the dorsal hippocampus and amygdaloid complex of the traumatized rats. NOS expression increased significantly in both the amygdaloid complex and dorsal hippocampus where the increase was statistically more prominent in the amygdaloid complex (p< 0.001) than in the dorsal hippocampus of the traumatized rats (p<0.05). Conclusion: Predator exposure in rats causes long-lasting anxiogenic effects associated with increases in NOS and decreases in GluN1 expressions in brain areas related to PTSD symptoms and excitotoxicity. The results suggest that excitotoxicity occurs through other mechanisms rather than GluN1 receptors. Keywords: Predator scent test, nNOS, Glutamate, Calmodulin, Amygdala, Hippocampus