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Öğe Agomelatine pretreatment prevents development of hyperglycemia and hypoinsulinemia in streptozotocin-induced diabetes in mice(Wiley, 2019) Ozcan, Mete; Canpolat, Sinan; Bulmus, Ozgur; Ulker, Nazife; Tektemur, Ahmet; Tekin, Suat; Ozcan, SibelThe main objective of this study was to investigate potential effectiveness of agomelatine pretreatment in the prevention of diabetes itself and encephalopathy, with a focus on brain tissue oxidative stress and inflammatory processes in streptozotocin (STZ)-induced diabetic mice. Interleukine-1 beta (IL-1 beta) and TACR1 (NK1), which is a tachykinine receptor, were used for the investigation of inflammation in the brain regions including raphe nucleus, periaqueductal gyrus (PAG), amygdala, and nucleus accumbens. The effects of agomelatine on total antioxidant capacity were also evaluated. In the in vitro part of the study, the effects of agomelatine on cell viability were investigated in dorsal root ganglion (DRG) neurons. Fasting blood glucose levels were measured 72 h after STZ injection to determine the diabetic condition. Agomelatine pretreatment prevented both hyperglycemia and hypoinsulinemia in STZ-treated mice. When STZ was injected to induce diabetes in mice, neither hyperglycemia nor hypoinsulinemia was developed in agomelatine pretreated mice and 6 weeks after development of diabetes, agomelatine treatment significantly decreased levels of IL-1 beta mRNA in raphe nucleus and nucleus accumbens. TACR1 mRNA levels were lower in raphe nucleus, PAG, and amygdala of agomelatine-treated diabetic mice. The increase in total antioxidant capacity after agomelatine administration may responsible for its beneficial effect in the prevention of diabetes. We showed that agomelatine reversed high glucose-induced cell viability decreases in DRG neurons. Both the antihyperglycemic and antioxidant effects of agomelatine might have contributed to the DRG neuron viability improvement. In conclusion, agomelatine seems to both prevent development of diabetes and reverse the encephalopathic changes caused by diabetes.Öğe The effect of subarachnoid or epidural bupivacaine on the QTc and P-wave dispersion(2020) Ozcan, Sibel; Secen, Ozlem; Yildiz Altun, Aysun; Demirel, IsmailAim: Bupivacaine, which is widely used in neuraxial anesthesia, may lead to negative inotropic effect and arrhythmias. In this study, our objective is to evaluate the effects of bupivacaine on corrected QT interval (QTc) and P wave dispersion in epidural anesthesia and to compare them with those in spinal anesthesia. Material and Methods: Ninety patients (59 male, 31 female) who applied neuraxial anesthesia for unilateral inguinal hernia repair were randomly allocated into two groups: Group S (Spinal, n = 49), Group E (Epidural, n = 41). Neuraxial anesthesia was performed by bupivacaine in both groups. We calculated heart rate, QT interval, corrected QT interval and P wave dispersion from electrocardiography, before anesthesia and after the operation. Results: Postoperative QT interval was significantly longer than preoperative value in both groups (preoperative 0.388 sec in Group S and Group E versus, postoperative 0.407 sec in Group S and 0.397 sec in Group E), (p=0.001). Postoperative QTc prolongation was significantly higher in Group S, but there was no statistically significant difference between the groups (preoperative 0.418 sec versus, postoperative 0.424 sec in Group S), (p = 0.129). Preoperative and postoperative P wave dispersion value revealed no statistically significant differences in both inter- and intragroup comparisons. Conclusion: Bupivacaine caused a postoperative QTc interval prolongation in spinal and epidural anesthesia, which did not reach levels that were regarded as risky for ventricular arrhythmias despite being more prominent in the spinal anesthesia group compared with the epidural anesthesia groupÖğe Humanin's impact on pain markers and neuronal viability in diabetic neuropathy model(Taylor & Francis Ltd, 2024) Kelestemur, Muhammed Mirac; Bulut, Ferah; Bilgin, Batuhan; Hekim, Munevver Gizem; Adam, Muhammed; Ozcan, Sibel; Beker, Mustafa CaglarObjective This study investigates the impact of chronic humanin (HN) treatment on pain-related markers (NMDA, substance P, TRPV1, and IL-1 beta) in diabetic mice's dorsal root ganglia (DRG). Additionally, we assess the effects of HN on cellular viability in DRG neurons. Methods In vivo experiments involved 15 days of HN administration (4 mg/kg) to diabetic mice (n = 10). Protein levels of NMDA, IL-1 beta, TRPV1, and substance P were measured in diabetic DRG. In vitro experiments explored HN's impact on apoptosis and cellular viability, focusing on the JAK2/STAT3 pathway. Results Humanin significantly reduced the elevated expression of NMDA, IL-1 beta, TRPV1, and substance P induced by diabetes (p < .05). Furthermore, HN treatment increased cellular viability in DRG neurons through JAK2/STAT3 pathway activation (p < .05). Conclusion These findings highlight the significance of understanding mitochondrial function and pain markers, as well as apoptosis in diabetes. The study provides insights for managing the condition and its complications.Öğe Modulation of Neuronal Damage in DRG by Asprosin in a High-Glucose Environment and Its Impact on miRNA181-a Expression in Diabetic DRG(Springer, 2024) Adam, Muhammed; Ozcan, Sibel; Dalkilic, Semih; Tektemur, Nalan Kaya; Tekin, Suat; Bilgin, Batuhan; Hekim, Munevver GizemAsprosin, a hormone secreted from adipose tissue, has been implicated in the modulation of cell viability. Current studies suggest that neurological impairments are increased in individuals with obesity-linked diabetes, likely due to the presence of excess adipose tissue, but the precise molecular mechanism behind this association remains poorly understood. In this study, our hypothesis that asprosin has the potential to mitigate neuronal damage in a high glucose (HG) environment while also regulating the expression of microRNA (miRNA)-181a, which is involved in critical biological processes such as cellular survival, apoptosis, and autophagy. To investigate this, dorsal root ganglion (DRG) neurons were exposed to asprosin in a HG (45 mmol/L) environment for 24 hours, with a focus on the role of the protein kinase A (PKA) pathway. Expression of miRNA-181a was measured by using real-time polymerase chain reaction (RT-PCR) in diabetic DRG. Our findings revealed a decline in cell viability and an upregulation of apoptosis under HG conditions. However, pretreatment with asprosin in sensory neurons effectively improved cell viability and reduced apoptosis by activating the PKA pathway. Furthermore, we observed that asprosin modulated the expression of miRNA-181a in diabetic DRG. Our study demonstrates that asprosin has the potential to protect DRG neurons from HG-induced damage while influencing miRNA-181a expression in diabetic DRG. These findings provide valuable insights for the development of clinical interventions targeting neurotoxicity in diabetes, with asprosin emerging as a promising therapeutic target for managing neurological complications in affected individuals.Öğe Oxytocin activates calcium signaling in rat sensory neurons through a protein kinase C-dependent mechanism(Springer, 2014) Ayar, Ahmet; Ozcan, Mete; Alcin, Ergul; Serhatlioglu, Ihsan; Ozcan, Sibel; Kutlu, Selim; Kelestimur, HalukIn addition to its well-known effects on parturition and lactation, oxytocin (OT) plays an important role in modulation of pain and nociceptive transmission. But, the mechanism of this effect is unclear. To address the possible role of OT on pain modulation at the peripheral level, the effects of OT on intracellular calcium levels ([Ca2+](i)) in rat dorsal root ganglion (DRG) neurons were investigated by using an in vitro calcium imaging system. DRG neurons were grown in primary culture following enzymatic and mechanical dissociation of ganglia from 1- or 2-day-old neonatal Wistar rats. Using the fura-2-based calcium imaging technique, the effects of OT on [Ca2+](i) and role of the protein kinase C (PKC)-mediated pathway in OT effect were assessed. OT caused a significant increase in basal levels of [Ca2+](i) after application at the doses of 30 nM (n=34, p<0.01), 100 nM (n=41, p<0.001) and 300 nM (n=46, p<0.001). The stimulatory effect of OT (300 nM) on [Ca2+](i) was persistent in Ca2+-free conditions (n=56, p<0.01). Chelerythrine chloride, a PKC inhibitor, significantly reduced the OT-induced increase in [Ca2+](i) (n=28, p<0.001). We demonstrated that OT activates intracellular calcium signaling in cultured rat primary sensory neurons in a dose-and PKC-dependent mechanism. The finding of the role of OT in peripheral pain modification may serve as a novel target for the development of new pharmacological strategies for the management of pain.
