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    The Effects of Cisplatin on the Kidney Metabolism: Role of Ginkgo Biloba Extract
    (2004) Yilmaz, H. Ramazan; Işik, Bünyamin; Güleç, Mukaddes; Sö?üt, Sadik; Akyol, Ömer
    In this study, we aimed to examine whether antitumour drug cisplatin affect the metabolism of the kidney and consequently causes kidney damage and, Ginkgo biloba extract prevents this damage in rats. The experimental groups were as follows: Control group, Cisplatin-treated group (Cisplatin), and a group treated with Cisplatin plus Ginkgo biloba extract (GBE). The Cisplatin and Cisplatin+GBE groups were treated intraperitoneally with a single dose of 7 mg/kg body weight sisplatin at 4th day of the treatment. GBE was administrated at a dose of 100 mg/kg body weight orally, three days before and seven days after the treatment with cisplatin in the cisplatin+GBE group. Kidney tissues were taken 7 day after the cisplatin administration. The activities of kidney hexokinase (HK), glucose-6-phosphate dehydrogenase (G6PD), lactate dehydrogenase (LDH) and malate dehydrogenase (MDH) serum enzymes were determined in each sample. The results of the experiment demonstrated that HK, G6PD, LDH, and MDH activities were increased significantly in the cisplatin group compared with control group. HK and G6PD activities were increased significantly in the cisplatin group compared with control group. G6PD activity was increased significantly in the cisplatin+GBE group compared with cisplatin group, and LDH activity was decreased significantly in the cisplatin+GBE group compared with cisplatin group. From these results, it can be concluded that cisplatin may cause kidney damage through metabolic enzymes and, GBE may prevent damage caused by cisplatin.
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    Effects of hyaluronan on nitric oxide levels and superoxide dismutase activities in synovial fluid in knee osteoarthritis
    (Springer London Ltd, 2007) Kalacı, Aydıner; Yilmaz, H. Ramazan; Aslan, Bahadir; Soeguet, Sadik; Yanat, Ahmet Nedim; Uz, Efkan
    The aim of the present study was to evaluate the effects of hyaluronan (HA) on nitric oxide (NO) levels and superoxide dismutase (SOD) enzyme activities in synovial fluid (SF) in the treatment of patients with knee osteoarthritis (OA). SF samples were aspirated from OA patients before the commencement of the treatment (n=23) and 6 weeks after they were treated with HA products. NO levels and SOD activities were compared between the pre- and post-treatment of OA patients and of the control group (n=10). SF NO levels were significantly higher in patients with OA before the commencement of the treatment compared with the post-treatment (p < 0.001) and the control groups. The SF SOD activity of patients before the commencement of the treatment was lower than the values in the controls and post-treatment (p < 0.001). There is no significant correlation between SF NO and SOD levels and the radiographic changes of the OA knee according to Kellgren-Lawrence grading (p > 0.05). Also, the Western Ontario and McMaster Universities Osteoarthritis index (WOMAC) pain scores and physical function scores were gradually improved. These findings made us think that SF NO was a potent mediator in cartilage damage in OA, whereas SOD was an antioxidant mediator in the same process. Exogenous HA injections might reduce the NO levels and increase SOD activities in synovial fluid. These effects also do not seem to be dependent on the radiographic grading of the OA knee. More comprehensive studies are needed to clarify a possible clinical significance of this topic, and we suggest that this is an important area for further research into new treatment options.
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    The protective effect of N-acetylcysteine against cyclosporine A-induced hepatotoxicity in rats
    (John Wiley & Sons Ltd, 2008) Kaya, Hasan; Koc, Ahmet; Sogut, Sadik; Duru, Mehmet; Yilmaz, H. Ramazan; Uz, Efkan; Durgut, Ramazan
    The immunosuppressive agent cyclosporine A (CsA) has been reported to exert measurable hepatotoxic effects. One of the causes leading to hepatotoxicity is thought to be reactive oxygen radical formation. The aim of this study was to investigate the effects of N-acetylcysteine (NAC) treatment on CsA-induced hepatic damage by both analysing superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), aspartate aminotransferase (AST) and alanine transaminase (ALT) activities with malondialdehyde (MDA) and nitric oxide (NO) levels, and using an histological approach. CsA administration produced a decrease in hepatic SOD activity, and co-administration of NAC with CsA resulted in an increase in SOD activity. MDA and NO levels increased in the CsA group and NAC treatment prevented those increases. A significant elevation in serum AST and ALT activities was observed in the CsA group, and when NAC and CsA were co-administered, the activities of AST and ALT were close to the control levels. CsA treatment caused evident morphological alterations. Control rats showed no abnormality in the cytoarchitecture of the hepatic parenchyma. The co-administration of NAC with CsA showed no signs of alteration and the morphological pattern was almost similar to the control group. In conclusion, CsA induced liver injury and NAC treatment prevented the toxic side effects induced by CsA administration through the antioxidant and radical scavenging effects of NAC. Copyright (C) 2007 John Wiley & Sons, Ltd.