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    Accumulation of ?-Synuclein in Cerebellar Purkinje Cells of Diabetic Rats and Its Potential Relationship with Inflammation and Oxidative Stress Markers
    (Hindawi Ltd, 2017) Solmaz, Volkan; Ozlece, Hatice Kose; Eroglu, Huseyin Avni; Aktug, Huseyin; Erbas, Oytun; Taskiran, Dilek
    Objective. The present study was conducted to evaluate the relationship between plasma oxidative stress markers such as malondialdehyde (MDA) and glutathione (GSH), inflammatory marker pentraxin-3 (PTX3), and cerebellar accumulation of alpha-synuclein in streptozotocin-(STZ-) induced diabetes model in rats. Methods. Twelve rats were included in the study. Diabetes (p = 6) was induced with a single intraperitoneal injection of streptozotocin (STZ, 60 mg/kg). Diabetes was verified after 48 h by measuring blood glucose levels. Six rats served as controls. Following 8 weeks, rats were sacrificed for biochemical and immunohistochemical evaluation. Results. Plasma MDA levels were significantly higher in diabetic rats when compared with the control rats (p < 0.01), while plasma GSH levels were lower in the diabetic group than in the control group (p < 0.01). Also, plasma pentraxin-3 levels were statistically higher in diabetic rats than in the control rats (p < 0.01). The analysis of cerebellar alpha-synuclein immunohistochemistry showed a significant increase in alpha-synuclein immunoexpression in the diabetic group compared to the control group (p < 0.01). Conclusion. Due to increased inflammation and oxidative stress in the chronic period of hyperglycemia linked to diabetes, there may be alpha-synuclein accumulation in the cerebellum and the plasma PTX3 levels may be assessed as an important biomarker of this situation.
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    Evaluation of long-term effects of artificial sweeteners on rat brain: a biochemical, behavioral, and histological study
    (Wiley, 2018) Erbas, Oytun; Erdogan, Mumin Alper; Khalilnezhad, Asghar; Solmaz, Volkan; Gurkan, Fulya Tuzcu; Yigitturk, Gurkan; Eroglu, Huseyin Avni
    The aim of the present study was to compare the effects of artificial sweeteners (aspartame, saccharin, and sucralose) on rat brain. Twenty-four adult male Sprague-Dawley rats were included in the study. The control group (n = 6) received regular tap water, whereas other groups received aspartame (3mg/kg/day, n = 6,) or saccharin (3mg/kg/day, n = 6) or sucralose (1.5mg/kg/day, n = 6) in the drinkingwater. Following 6weeks, the passive avoidance learning (PAL) test was performed to evaluate the neurobehavioral effects of sweeteners. The brains were assessed for lipid peroxides, neuron count, and Glial fibrillary acidic protein (GFAP) immunohistochemistry. Our results demonstrated that chronic intake of sweeteners significantly impaired PAL performance in all groups. Hippocampal CA1-CA3 areas revealed significantly lower neuronal count in aspartame and increased GFAP expression in all groups. Brain lipid peroxides were significantly higher in all groups. Our findings suggest that long-term consumption of artificial sweeteners may have harmful effects on cognition and hippocampal integrity in rats.
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    Highly selective SGLT2 inhibitor dapagliflozin reduces seizure activity in pentylenetetrazol-induced murine model of epilepsy
    (Biomed Central Ltd, 2018) Erdogan, Mumin Alper; Yusuf, Dimas; Christy, Joanna; Solmaz, Volkan; Erdogan, Arife; Taskiran, Emin; Erbas, Oytun
    Background: Worldwide, over 10 million individuals suffer from drug-resistant epilepsy. New therapeutic strategies are needed to address this debilitating disease. Inhibition of sodium-glucose linked transporters (SGLTs), which are variably expressed in the brain, has been demonstrated to reduce seizure activity in murine models of epilepsy. Here we investigated the effects of dapagliflozin, a highly competitive SGLT2 inhibitor currently used as a drug for diabetes mellitus, on seizure activity in rats with pentylenetetrazol (PTZ) induced seizures. Methods: Laboratory rats (n = 48) were evenly randomized into two experiments, each with four study arms: (1) a vehicle-treated (placebo) arm infused with saline; (2) a control arm infused with PTZ; (3) a treatment arm with PTZ and dapagliflozin at 75 mg/kg, and (4) another treatment arm with PTZ and dapagliflozin at 150 mg/kg. Study subjects were assessed for seizures either via EEG as measured by spike wave percentage (SWP), or clinically via Racine's scales scores (RSS) and time to first myoclonic jerk (TFMJ). Results: Rats treated with dapagliflozin had lower mean SWP on EEG (20.4% versus 75.3% for untreated rats). Behaviorally, treatment with dapagliflozin improved means RSS (2.33 versus 5.5) and mean TFMJ (68.3 versus 196. 7 s). All of these findings were statistically significant with p-values of < 0.0001. There was a trend towards even better seizure control with the higher dose of dapagliflozin at 150 mg/kg, however this was not consistently statistically significant. Conclusions: Dapagliflozin decreased seizure activity in rats with PTZ-induced seizures. This may be explained by the anti-seizure effects of decreased glucose availability and a reduction in sodium transport across neuronal membranes which can confer a stabilizing effect against excitability and unwanted depolarization. The potential clinical role of dapagliflozin and other SGLT2 inhibitors as anti-seizure medications should be further explored.
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    Inhibitor effect of paricalcitol in rat model of pentylenetetrazol-induced seizures
    (Springer, 2016) Uyanikgil, Yigit; Solmaz, Volkan; Cavusoglu, Tuerker; Cinar, Bilge Piri; Cetin, Emel Oeykue; Sur, Halil YAñlmaz; Erbas, Oytun
    Vitamin D has various systemic effects on bone metabolism, modulation of the immune system, stabilization of the cell membrane, oxidative stress, inflammation, apoptosis, and various other hormones. Differing from active vitamin D, paricalcitol is a relatively safe VDR agonist due to its relatively few side effects. This study has investigated the anticonvulsant effect of paricalcitol in convulsions induced by pentylenetetrazole (PTZ). 36 male Sprague-Dawley rats were divided randomly into two groups: 18 for EEG recording (PTZ 35 mg/kg) and 18 for behavioral studies (PTZ 70 mg/kg). Forty-five minutes before the PTZ injection, both groups of rats were given 5 and 10 mu g/kg of paricalcitol i.p., respectively. Racine convulsion scores, first myoclonic jerk time, spike percentages, and antioxidant status were evaluated in the groups. Our results showed that the Racine's Convulsion Scale (RCS) score significantly dropped in the paricalcitol-treated group, analysis of the first myoclonic jerk (FMJ) latencies demonstrated a significantly longer latency in the paricalcitol-applied group, and spike percentages at EEG recordings significantly decreased with paricalcitol. Moreover, MDA levels were lower and SOD activity were higher in the 5 mu g/kg paricalcitol group compared to the saline group; these results were more prominent in 10 mu g/kg paricalcitol group. Our study has demonstrated that paricalcitol has protective effects on PTZ-induced convulsions. Based on the SOD and MDA levels in our study, these effects may result from the antioxidant characteristics of paricalcitol.
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    Neuroprotective Effects of Eexenatide in a Rotenone-Induced Rat Model of Parkinson's Disease
    (Elsevier Science Inc, 2017) Aksoy, Durdane; Solmaz, Volkan; Cavusoglu, Turker; Meral, Ayfer; Ates, Utku; Erbas, Oytun
    Backround: Several studies suggest an association between Parkinson's disease (PD) and type 2 diabetes mellitus; these 2 diseases are both known to affect the common molecular pathways. As a synthetic agonist for the glucagon-like peptide 1 receptor, exenatide has been evaluated as a neuroprotective agent in multiple animal models. Rotenone models of PD have great potential for the investigation of PD pathology and motor and nonmotor symptoms, as well as the role of gene environment interactions in PD causation and pathogenesis. Therefore, in this study, the neurochemical, behavioral and histologic effects of exenatide on a rotenone-induced rat model of PD were examined. Materials and Methods: Eighteen adult male rats were randomly divided into the following 3 groups (n = 6): 1 group received stereotaxical infusion of dimethyl sulfoxide (vehicle, group 1) and the others received stereotaxical infusion of rotenone (groups 2 and 3). Apomorphine-induced rotation test was applied to the rats after 10 days. Thereafter, group 2 was administered isotonic saline, whereas group 3 was administered exenatide for 28 days. Results: Malondialdehyde and tumor necrosis factor alpha levels increased in the rats with PD induced by rotenone, whereas malondialdehyde and tumor necrosis factor alpha levels markedly decreased in the rats treated with exenatide. The apomorphine-induced rotation test scores of exenatide-treated rats were determined to be lower compared with the untreated group. Additionally, treatment with exenatide significantly reduced the loss of dopaminergic neurons in striatum. Conclusions: These results have shown that exenatide has neuroprotective, anti-inflammatory and antioxidant effects in a rotenone-induced rat model of PD.
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    Neuroprotective effects of octreotide on diabetic neuropathy in rats
    (Elsevier France-Editions Scientifiques Medicales Elsevier, 2017) Solmaz, Volkan; Cinar, Bilge Piri; Yigitturk, Gurkan; Ozlece, Hatice Kose; Eroglu, Huseyin Avni; Tekatas, Aslan; Erbas, Oytun
    The purpose of the present study is to investigate the possible healing effects of octreotide (OCT) on motor performance, electrophysiological and histopathological findings of diabetic neuropathy in a rat model of diabetes mellitus (DM). To induce diabetes, rats were administered a single dose (60 mg/kg) of streptozotocin (STZ). Diabetic rats were treated either with saline (1 ml/kg/day, n = 7) or OCT (0.1 mg/kg/ day, n = 7) for four weeks. Seven rats served as control group and received no treatment. At the end of the study, electromyography (EMG), gross motor function (inclined plate test), general histology and the perineural thickness of sciatic nerve were evaluated. At the end of study, weight loss was significantly lower in OCT treated rats than that of saline treated ones (p < 0.001). Electrophysiologically, compound muscle action potential (CMAP) amplitudes of the saline treated DM group were significantly reduced than those of controls (p < 0.0001). Also, distal latency and CMAP durations were significantly prolonged in saline treated DM group (p < 0.05) compared to control. However, treatment of diabetic rats with OCT significantly counteracted these alterations in EMG. Furthermore, OCT significantly improved the motor performance scores in diabetic rats (p < 0.05). Histomorphometric assessment of the sciatic nerve demonstrated a significant reduction in perineural thickness in OCT treated group compared to saline group. In conclusion, OCT possesses beneficial effects against STZ-induced diabetic neuropathy, which promisingly support the use of OCT as a neuroprotective agent in patients with diabetic neuropathy. (C) 2017 Elsevier Masson SAS. All rights reserved.