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Öğe Effects of ceftriaxone on ischemia/reperfusion injury in rat brain(Elsevier Sci Ltd, 2013) Altas, M.; Meydan, S.; Aras, M.; Yilmaz, N.; Ulutas, K. T.; Okuyan, H. M.; Nacar, A.The aim of this study was to investigate the effect of ceftriaxone treatment against short-term global brain ischemia/reperfusion (I/R) injury in rats. The study was carried out on 30 Wistar-albino rats that were divided into three groups: control group (n = 10), I/R group (n = 10) and I/R-ceftriaxone group (n = 10). Malondialdehyde (MDA) levels were significantly increased in the I/R group in comparison with the control group (p < 0.001). MDA was significantly lower in the I/R-ceftriaxone group than in the I/R group (p < 0.05). Superoxide dismutase activity was significantly decreased in the I/R group and increased in the I/R-ceftriaxone group as compared with the control group. Glutathione peroxidase activity was significantly decreased in the I/R group and increased in the I/R-ceftriaxone group as compared with the I/R group and the control. Histopathologically, ceftriaxone provided morphological improvement compared with the I/R group. We concluded that ceftriaxone has neuron-protective effects due to its antioxidant properties as shown by a decrease in MDA overproduction and histological improvement in brain tissue. (C) 2012 Elsevier Ltd. All rights reserved.Öğe Effects of erdosteine on cyclosporin-A-induced nephrotoxicity(Sage Publications Ltd, 2012) Tutanc, M.; Arica, V.; Yilmaz, N.; Nacar, A.; Zararsiz, I.; Basarslan, F.; Tutanc, O. D.Aim: In cyclosporin-A (CsA)-induced toxicity, oxidative stress has been implicated as a potential responsible mechanism. Therefore, we aimed to investigate the protective role of erdosteine against CsA-induced nephrotoxicity in terms of tissue oxidant/antioxidant parameters and light microscopy in rats. Materials and methods: Wistar albino rats were randomly separated into four groups. Group I rats treated with sodium chloride served as the control, group 2 rats were treated with CsA, group 3 with CsA plus erdosteine, and group 4 with erdosteine alone. Animals were killed and blood samples were analyzed for blood urea nitrogen (BUN), serum creatinine (Cr), uric acid (UA), total protein (TP), and albumin (ALB) levels. Kidney sections were analyzed for malondialdehyde (MDA) and nitric oxide (NO) levels and superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities, as well as for histopathological changes. Results: In the CsA group, MDA, GSH-Px, BUN, and Cr levels were increased. The TP and ALB levels were decreased. These changes had been improved by erdosteine administration. Other biochemical parameters did not show any significant change. Conclusion: These results indicate that erdosteine produces a protective mechanism against CsA-induced nephrotoxicity and suggest a role of oxidative stress in pathogenesis.Öğe Investigation of liposome formulation effects on rivastigmine transport through human colonic adenocarcinoma cell line (CACO-2)(2010) De?im, Z.; Mutlu, N.B.; Yilmaz, Ş.; Eşsiz, D.; Nacar, A.Transportations of rivastigmine containing liposomes across Caco-2 cells were studied and in vitro test results were compared with in vivo results. MTT test was used for cell viability studies. Series of formulations were prepared containing rivastigmine which is used for the treatment of Alzheimer's disease. Characterization and stability studies for liposome formulations were performed. Encapsulation efficiencies of liposomes were 35.4%, 25.2% and 29.9% for rivastigmine, rivastigmine-sodium taurocholate, rivastigmine-dimethylbeta-CD liposomes, respectively. In stability studies, particle size and size distribution, zeta potential, rivastigmine amounts were determined and shelf lives of liposomes were calculated. Penetration properties of rivastigmine through Caco-2 cells, dialysis membrane and kinetics of release from liposomes were determined. Permeability coefficients were calculated after diffusion studies. The highest value of % cumulative amount of rivastigmine passed through caco-2 cell cultures was found to be 87.2% for rivastigmine-sodium taurocholate solution and 12.8% for rivastigmine-sodium taurocholate liposome. The highest permeability coefficient value was obtained with sodium taurocholate liposomes for -0.75. Rivastigmine liposomes and solutions were also applied to animals. Acetyl choline esterase (AChE) activity was determined by the Ellman method on mice. %AChE inhibition values were calculated using blood and brain tissue samples. The physical appearances of the brains were investigated by TEM microscope. The highest value of AChE inhibition was observed for rivastigmine and sodium taurocholate liposomes. The histological investigations and observations also supported these results.Öğe Protective effect of ebselen on experimental testicular torsion and detorsion injury(Wiley, 2014) Rifaioglu, M. M.; Motor, S.; Davarci, I.; Tuzcu, K.; Sefil, F.; Davarci, M.; Nacar, A.Ebselen is used as a drug in clinical trials against stroke, reperfusion injury with anti-atherosclerotic and renoprotective effects. The aim of this study is to investigate the protective effect of ebselen, on torsion/detorsion (T/D)-induced biochemical and histopathological changes in experimental testicular ischaemia/reperfusion injury. A total of 28 male Wistar Albino rats were divided into four groups: group 1(sham-operated group, n=7), group 2(ebselen group, n=7), group 3(torsion/detorsion + saline, n=7) and group 4(T/D+10mgkg(-1) ebselen group, n=7). The tissue homogenate samples were used for immediate nitric oxide (NO), malondialdehyde (MDA), superoxide dismutase, catalase and glutathione measurement. Testes in all groups were evaluated for the biochemical assay and histopathological examinations. To evaluate spermatogenesis, Johnsen scoring system was used. Testicular tissue MDA and NO levels in group 3 were significantly higher than in group 1 and 4. In histological evaluation of the testicular tissues, ebselen administration improved tubular histology significantly compared with T/D group. Significant increase in histological score was observed in the testis of group 3 compared with group 1 and 2. Histological score in group 4 significantly decreased compared with group 3. Johnson score was significantly lower in T/D group compared with all other three groups, ebselen administration increased the score significantly compared with T/D group. Ebselen reduced oxidative biochemical and histopathological damage in our testicular T/D rat model.Öğe The protective effects of omega-3 fatty acid against toluene-induced neurotoxicity in prefrontal cortex of rats(Sage Publications Ltd, 2012) Meydan, S.; Altas, M.; Nacar, A.; Ozturk, O. H.; Tas, U.; Zararsiz, I.; Sarsilmaz, M.Objective: Toluene is used as an organic solvent, and it has neurotoxic effects. Omega-3 is an essential fatty acid required for brain development. The aim of this study was to investigate the protective effects of omega-3 fatty acid against toluene-induced neurotoxicity in prefrontal cortex of rats. Materials and methods: A total of 21 male Wistar rats were divided into three groups with seven rats in each group. Rats in group I were the controls. Toluene was intraperitoneally injected into the rats of group II with a dose of 0.5 ml/kg. Rats in group III received omega-3 fatty acid with a dose of 0.4 g/kg/day while exposed to toluene. After 14 days, all the rats were killed by decapitation. Enzymatic activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) and the level of malondialdehyde (MDA) were spectrophotometrically studied in the prefrontal cortex of rats. Results: Enzymatic activities of SOD and GSH-Px were decreased, and MDA levels were significantly increased in rats treated with toluene compared with the controls. However, the increased SOD and decreased GSH-Px enzymatic activities and MDA levels were detected in the rats administered with omega-3 fatty acid while exposed to toluene. Conclusion: The results of this experimental study indicate that omega-3 fatty acid treatment can prevent toluene-induced neuronal damage in the prefrontal cortex of rats.
