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    Effects of caffeic acid phenethyl ester on thioacetamide-induced hepatic encephalopathy in rats
    (Pergamon-Elsevier Science Ltd, 2010) Fadillioglu, Ersin; Gursul, Cebrail; Iraz, Mustafa
    Hepatic encephalopathy (HE) is a major neurological complication secondary to severe liver failure. The aim of the present study was to examine the possible neuroprotective effects of caffeic acid phenethyl ester (CAPE) with or without laxative treatment against thioacetamide-induced HE by investigating behavioral and motor activities in rats as well as blood ammonia level and oxidant-antioxidant parameters of cortex, brain stem and cerebellum. After induction of HE by thioacetamide, the rats were treated with lactulose, CAPE (CAPE treatment was started one day before the first dose of thioacetamide) or CAPE plus lactulose. The behavioral and motor scales were measured at the 54th hour after the first thioacetamide injection, the blood samples and brains were taken under anesthesia at the 60th hour for biochemical analysis. The survival rates were 37.5% in HE group, 70% in HE + lactulose group, 80% in HE + CAPE group, and 100% in HE + CAPE + lactulose group. Increased ammonia, ALT and AST levels in blood along with impaired sensory-motor behavior tests were reversed to proximate control values in CAPE + lactulose treated group. There were increased lipid peroxidation and protein oxidation and decreased antioxidant enzyme activities in almost all brain parts of HE group. CAPE or lactulose treatment alone ameliorated those oxidant and antioxidant parameters; however, CAPE treatment together with lactulose reversed them to almost control level. In conclusion, thioacetamide-induced HE injury in rats was reversed almost fully by CAPE and laxative combination. There was no death in CAPE and laxative treated group animals and it may be due to the direct neuroprotective effect of CAPE together with the prevention of the body from ammonia production. (C) 2010 Elsevier Inc. All rights reserved.
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    Effects of melatonin treatment on the spermatogenesis and serum inflammatory cytokine levels in diabetic rats
    (2018) Bozkurt, Aliseydi; Karabakan, Mehmet; Aydin, Merve; Gumustas, Sinem; Onk, Didem; Gursul, Cebrail; Erol, Huseyin Serkan
    Aim: Diabetes mellitus (DM) is known to have side effects on sexual and reproductive functions in males. The aim of current study was to investigate the effect of melatonin treatment on spermatogenesis and serum inflammatory cytokine levels in diabetic rats. Material and Method: Eighteen adult Wistar albino male rats were divided randomly into three groups each containing 6 rats; control group (group 1), diabetic group (group 2), diabetic treated with melatonin group (group 3). Experimental diabetes was obtained by administrating 50 mg/kg streptozotocin. Melatonin treatment was administered intraperitoneally for 7 days at a dose of 20 mg, daily. Serum levels of interleukin-1 beta (IL-1β), interleukin 6 (IL-6) and tumor necrosis factor-alpha (TNF-α) were assayed. Spermatogenesis was evaluated according to Johnsen score at immunopathological examination.Results: The Johnsen scores in control, diabetic and treatment groups were 9.78, 8.91, and 9.61, respectively. Spermatogenesis was negatively affected in diabetic rats and significantly improved with melatonin therapy (p0.05). The serum levels of TNF-α in diabetic rats were observed to be increased compared to the control group (p0.05). The levels of serum IL-1β and TNF- α were significantly decreased with melatonin treatment. IL-6 levels were not different among the three groups (p=0.248). Conclusions: In the present study, intraperitoneal melatonin treatment was determined to have a positive effect of on spermatogenesis and caused a decrease in serum inflammatory cytokine levels in diabetic rats.Keywords: Cytokines; Diabetes Mellitus; Melatonin; Rats; Spermatogenesis.
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    Melatonin treatment against remote organ injury induced by renal ischemia reperfusion injury in diabetes mellitus
    (Pharmaceutical Soc Korea, 2008) Fadillioglu, Ersin; Kurcer, Zehra; Parlakpinar, Hakan; Iraz, Mustafa; Gursul, Cebrail
    Oxidative stress may have a role in liver damage after acute renal injury due to various reasons such as ischemia reperfusion (IR). Diabetes mellitus (DM) is an important disease for kidneys and may cause nephropathy as a long term complication. The aim of this study was to investigate protective effect of melatonin, a potent antioxidant, against distant organ injury on liver induced by renal IR in rats with or without DM. The rats were divided into six groups: control (n=7), DM (n=5), IR (n=7), DM+IR (n=7), melatonin+IR (Mel+IR) (melatonin, 4 mg/kg during 15 days) (n=7), and Mel+DM+IR groups (n=7). Diabetes developed 3 days after single i.p. dose of 45 mg/kg streptozotocin. After 15 day, the left renal artery was occluded for 30 min followed 24 h of reperfusion in IR performed groups. DM did not alter oxidative parameters alone in liver tissue. The levels of malondialdehyde, protein carbonyl and nitric oxide with activities of xanthine oxidase and myeloperoxidase were increased in liver tissues of diabetic and non-diabetic IR groups. Nitric oxide level in DM was higher than control. The activities of catalase and superoxide dismutase were increased in IR groups in comparison with control and DM. ALT and AST levels were higher in IR and DM+IR groups than control and DM. Melatonin treatment reversed all these oxidant and antioxidant parameters to control values as well as serum liver enzymes. We concluded that renal IR may affect distant organs such as liver and oxidative stress may play role on this injury, but DM has not an effect on kidney induced distant organ injury via oxidant stress. Also, it was concluded that melatonin treatment may prevent liver oxidant stress induced by distant injury of kidney IR.
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    The preventive role of medical ozone therapy on remote organ injury induced by hepatic ischemia reperfusion
    (2021) Demirtas, Levent; Gursul, Cebrail; Gurbuzel, Ahmet; Sayar, Ilyas; Gurbuzel, Mehmet; Bicer, Senol; Akbas, Emin Murat
    Aim: This study explores the effects of ozone therapy on the prevention of remote organ injury in rats with induced hepatic ischemia reperfusion injury. Materials and Methods: Twenty-one male Sprague Dawley rats were sorted randomly into three groups: (a) A control group in which the rats’ abdomens were operated on by laparotomy, and their livers then viewed and closed with a suture; (b) Rats with induced hepatic ischemia-reperfusion injuries; and (c) Rats induced with the same injuries that were administered ozone therapy before reperfusion. The rats’ hepatic arteries, portal veins, and bile ducts were clamped, and ischemia was induced for 45 min. Reperfusion was provided for 90 min in the second and third groups. The third group was administered 0.5 mg/kg ozone intraperitoneally before reperfusion. Liver, lung, and kidney tissues were taken for biochemical and histopathological examinations. Results: In the second group, malondialdehyde levels in the lung and kidney tissues were higher than in the control group, while catalase and superoxide dismutase enzyme levels were lower. The third group had lower malondialdehyde levels and higher catalase and superoxide dismutase enzyme levels than the group that did not receive the therapy. In histopathological evaluations, the damage to both kidney and lung tissues in the third group was higher than in the control group; however, this damage was significantly lower than in the second group. Conclusions: The findings indicated that the administration of ozone therapy attenuated lung and kidney injuries caused by hepatic ischemia, since partial protection was demonstrated in many instances.