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    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, Sibel
    The 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.
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    Apelin has inhibitory effect of endothelium-independent relaxation in the human internal mammary artery
    (2019) Kacar, Emine; Burma, Oktay; Serhatlioglu, Ihsan; Ulker, Nazife; Uysal, Ayhan; Yardimci, Ahmet; Kelestimur, Haluk
    Aim: Apelin has important effects on the circulatory system and heart. The main aim of this study was to investigate the effects of apelin-13 on the contraction induced by norepinephrine (NE), and the endothelium-independent relaxation induced by sodium nitroprusside (SNP) in human internal mammary artery (IMA) obtained from patients undergoing coronary artery bypass grafting (CABG) surgery. Material and Methods: IMA rings, obtained from patients undergoing CABG surgery, were suspended in isolated tissue baths containing Krebs-Henseleit solution, which were continuously gassed with 95% O2 and 5% CO2 at 37°C. Results: The IMA rings were pre-contracted with increasing concentrations of norepinephrine (NE 10-9–10-4 mol/l) and the endothelium-independent relaxation responses to sodium nitroprusside (SNP) were studied. Apelin-13 (10 μM) caused a dosedependent relaxation in NE pre-contracted IMA rings. Apelin also facilitated the endothelium-independent relaxation induced by SNP. Conclusion: According to the results, apelin facilitated the endothelium-independent relaxation and inhibited the contractile activity of IMA. These results suggest that apelin may be a physiological agent against the deterioration of vascular elasticity caused by endothelial damage especially in atherosclerotic cardiac patients and hypertensive patients.