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Öğe Antiepileptogenic and antioxidant effects of Nigella sativa oil against pentylenetetrazol-induced kindling in mice(Pergamon-Elsevier Science Ltd, 2005) Ilhan, A; Gurel, A; Armutcu, F; Kamisli, S; Iraz, MNigella sativa oil (NSO), a herbaceous plant, has been used for thousands of years for culinary and medical purposes. This study aimed to investigate the anticonvulsant and antioxidant activities of NSO on pentylenetetrazol (PTZ) kindling seizures in mice. Nigella sativa oil was tested for its ability (i) to suppress the convulsive and lethal effects of PTZ in kindled mice (anti-epileptogenic effect), (ii) to attenuate the PTZ-induced oxidative injury in the brain tissue (antioxidant effect) when given as a pretreatment prior to each PTZ injection during kindling acquisition. Valproate, a major antiepileptic drug, was also tested for comparison. Both substances studied significantly decreased oxidative injury in the mouse brain tissue in comparison with the PTZ-kindling group. Nigella sativa oil was found to be the most effective in preventing PTZ-induced seizures relative to valproate. Nigella sativa oil showed anti-epileptogenic properties as it reduced the sensitivity of kindled mice to the convulsive and lethal effects of PTZ; valproate was ineffective in preventing development of any of these effects. The data obtained support the hypothesis that neuroprotective action of NSO may correlate with its ability to inhibit not only excessive reactive oxygen species (ROS) formation but also seizure generation. (c) 2005 Elsevier Ltd. All rights reserved.Öğe Caffeic acid phenethyl ester exerts a neuroprotective effect on CNS against pentylenetetrazol-induced seizures in mice(Kluwer Academic/Plenum Publ, 2004) Ilhan, A; Iraz, M; Gurel, A; Armutcu, F; Akyol, OSince overexcitation of excitatory amino acid is an important mechanism in seizure genesis wherein free radicals have recently been suggested to play a critical role, we explored the effects of caffeic acid phenethyl ester (CAPE) administration in pentylenetetrazole (PTZ)-induced seizure in mice. CAPE prevents the oxidative damage in brain tissue induced by PTZ, scavenging reactive oxygen species (ROS). Our results demonstrate that CAPE treatment which prevents free radical production and ameliorates seizure severity may be useful at least as an adjunctive treatment of seizure disorders.Öğe Effect of long-term therapy with sodium valproate on nail and serum trace element status in epileptic children(Humana Press Inc, 2004) Armutcu, F; Ozerol, E; Gurel, A; Kanter, M; Vural, H; Yakinci, C; Akyol, OAntiepileptic drugs could cause changes in the trace element status of the body. Valproic acid (VPA) is a very effective anticonvulsant agent widely used in the management of various forms of epilepsy. Nail trace element content is a reliable index of trace element nutritional status of the body. To determine whether some of the side effects of antiepileptic drugs could be the result of zinc (Zn) depletion within tissues, Zn concentrations as well as copper (Cu) concentrations in nail and serum in 59 children having various types of epilepsy receiving valproate and 31 controls were assessed. Although serum Zn level in epileptic patients was found to be decreased, there was no difference in nail samples when compared to controls. There was a statistically significant increase in nail Cu level in epileptic patients when compared to controls. On the other hand, serum Cu levels were not different between the groups. Although none of our patients showed any symptoms of Cu elevation and Zn depletion, we should pay attention to potential body trace element changes in patients with epilepsy under VPA treatment. In conclusion, our results indicate that serum trace metal homeostasis might be affected by VPA therapy, but not by the convulsive disorder itself.Öğe Effects of aminoguanidine and antioxidant erdosteine on bleomycin-induced lung fibrosis in rats(Academic Press Inc Elsevier Science, 2004) Yildirim, Z; Turkoz, Y; Kotuk, M; Armutcu, F; Gurel, A; Iraz, M; Ozen, SReactive oxygen and nitrogen species have been implicated in the pathogenesis of bleomycin -induced lung fibrosis. The effects of aminoguanidine and erdosteine on the bleomycin-induced lung fibrosis were evaluated in rats. The animals were placed into five groups: Vehicle + vehicle, vehicle + bleomycin (2.5U/kg), bleomycin + aminoguanidine (200mg/kg), bleomycin + erdosteine (10mg/kg), and bleomycin + erdosteine + aminoguanidine. Bleomycin administration resulted in prominent lung fibrosis as measured by lung hydroxyproline content and lung histology, which is completely prevented by erdosteine and aminoguanidine. A strong staining for nitro tyrosine antibody in lung tissue and increased levels of lung NO were found in bleomycin group, that were significantly reduced by aminoguanidine and erdosteine. Aminoguanidine and erdosteine significantly prevented depletion of superoxide dismutase and glutathione peroxidase and elevated myeloperoxidase activities, malondialdehyde level in lung tissue produced by bleomycin. Data presented here indicate that aminoguanidine and erdosteine prevented bleomycin-induced lung fibrosis and that nitric oxide mediated tyrosine nitration of proteins plays a significant role in the pathogenesis of bleomycin-induced lung fibrosis. Also our data suggest that antifibrotic affect of antioxidants may be due to their inhibitory effect on nitric oxide generation in this model. (C) 2004 Elsevier Inc. All rights reserved.Öğe Erdosteine ameliorates neurological outcome and oxidative stress due to ischemia/reperfusion injury in rabbit spinal cord(W B Saunders Co Ltd, 2004) Ege, E; Ilhan, A; Gurel, A; Akyol, O; Ozen, SObjective. Oxygen-derived free radicals have been suggested as important in degeneration after spinal cord ischemia. The aim of this study was to investigate whether erdosteine has a protective effect against spinal cord ischemia during aortic cross clamping. Materials and methods. New Zealand White rabbits (n = 21) were divided into three groups. In the ischemia/reperfusion group (I/R) (n = 8), the infrarenal aorta of rabbits was cross clamped for 21 min and then reperfused. In erdosteine group, the administration of erdosteine solution (50 mg/kg) was started two days before aortic cross-clamping and rabbits (n = 8) were subjected to ischemia and reperfusion. Animals in control group (n = 5) underwent a surgical procedure similar to the other groups but the aorta was not clamped. The animals were sacrificed at 72 h and histopathological, and biochemical analyses were carried out on the lumbar spinal cords. Results. Erdosteine treatment zoos associated with improved neurological function in the postoperative period. Histopathological examination of spinal cord tissues in erdosteine group revealed changes consistent with mild ischemic injury, but rabbits in I/R group with paraplegia had total destruction of the motor neurons. Biochemical analyses of spinal cord tissues, in the I/R group, revealed a significant increase in the superoxide dismutase, xanthine oxidase, adenosine deaminase and myeloperoxidase activities, and a significant depletion in glutathione peroxidase activity when compared to that of control rabbits. Erdosteine treatment prevented the increase of all these enzymes except adenosine deaminase. Ischemia/reperfusion produced a significant increase in the tissue malondialdehyde levels. Ischemia/reperfusion-induced increments in malondialdehyde content of the spinal cord were significantly prevented by erdosteine treatment. Conclusions. The present study demonstrated that erdosteine treatment before aortic cross clamping ameliorates neurological outcome, neuronal injury and oxidative stress in the rabbit spinal cord.Öğe Erdosteine ameliorates PTZ-induced oxidative stress in mice seizure model(Pergamon-Elsevier Science Ltd, 2005) Ilhan, A; Aladag, MA; Kocer, A; Boluk, A; Gurel, A; Armutcu, FThe role of oxygen-derived free radicals has been suggested in genesis of epilepsy and in the post seizure neuronal death. The aim of this study was to investigate whether erdosteine has a preventive effect against epilepsy and postepileptic oxidative stress. The mice (n = 27) were divided into three groups: (i) PTZ-induced-epilepsy group (it = 9); (ii) PTZ-induced-epilepsy + erdosteine group (it = 9); (iii) control group (n = 9). The animals were observed for a period of 30 min for latency to first seizure onset, total seizure duration, the number of seizure episodes. Then they were sacrificed and the brains were quickly removed, and frozen for biochemical analysis. Malondialdehyde (MDA), nitric oxide (NO), superoxide dismutase (SOD) and xanthine oxidase (XO) activities were carried out in the brain tissue. The latent period between PTZ induction and seizure are longer in the PTZ + erdosteine group than in PTZ-induced-epilepsy group (P < 0.05). Biochemical analyses of brain tissue, revealed a significant increase in the MDA, XO and NO levels in the PTZ group according to erdosteine group. SOD level did not change in this group. While MDA and XO levels are significantly lower, SOD level is significantly higher in the PTZ + erdosteine group compared to PTZ and control groups (P < 0.01). The present study demonstrated that erdosteine treatment both may increase latent interval between seizures and may decrease oxidative stress, thus may ameliorate neuronal death in brain during seizures. It may be used as an adjunct therapy in epilepsy. (c) 2005 Elsevier Inc. All rights reserved.Öğe Ginkgo biloba prevents mobile phone-induced oxidative stress in rat brain(Elsevier, 2004) Ilhan, A; Gurel, A; Armutcu, F; Kamisli, S; Iraz, M; Akyol, O; Ozen, SBackground: The widespread use of mobile phones (MP) in recent years has raised the research activities in many countries to determine the consequences of exposure to the low-intensity electromagnetic radiation (EMR) of mobile phones. Since several experimental studies suggest a role of reactive oxygen species (ROS) in EMR-induced oxidative damage in tissues, in this study, we investigated the effect of Ginkgo biloba (Gb) on MP-induced oxidative damage in brain tissue of rats. Methods: Rats (EMR+) were exposed to 900 MHz EMR from NIP for 7 days (1 h/day). In the EMR + Gb groups, rats were exposed to EMR and pretreated with Gb. Control and Gb-administrated groups were produced by turning off the mobile phone while the animals were in the same exposure conditions. Subsequently, oxidative stress markers and pathological changes in brain tissue were examined for each groups. Results: Oxidative damage was evident by the: (i) increase in malondialdehyde (MDA) and nitric oxide (NO) levels in brain tissue, (ii) decrease in brain superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities and (iii) increase in brain xanthine oxidase (XO) and adenosine deaminase (ADA) activities. These alterations were prevented by Gb treatment. Furthermore, Gb prevented the MP-induced cellular injury in brain tissue histopathologically. Conclusion: Reactive oxygen species may play a role in the mechanism that has been proposed to explain the biological side effects of MP, and Gb prevents the MP-induced oxidative stress to preserve antioxidant enzymes activity in brain tissue. (C) 2003 Elsevier B.V. All rights reserved.Öğe Investigation of oxidant/antioxidant parameters in penthylenetetrazol-induced seizures in mice and the protective effect of erdosteine treatment(Dr Dietrich Steinkopff Verlag, 2004) Ilhan, A; Akyol, O; Armutcu, F; Iraz, M; Gurel, A[Abstract Not Available]Öğe The protective effect of nebivolol on ischemia/reperfusion injury in rabbit spinal cord(Pergamon-Elsevier Science Ltd, 2004) Ilhan, A; Yilmaz, HR; Armutcu, F; Gurel, A; Akyol, OThe aim of this experimental study was to investigate whether nebivolol has protective effects against neuronal damage induced by spinal cord ischemia/reperfusion (I/R). Twenty-one rabbits were divided into three groups: group I (control, no I/R), group II (only I/R) and group III (I/R+nebivolol). Spinal cord ischemia was induced by clamping the aorta both below the left renal artery and above the aortic bifurcation. Seventy-two hours postoperatively, the motor function of the lower limbs was evaluated in each animal. The animals were sacrificed at 72 h, and histopathological and biochemical analyses were carried out in the lumbar spinal cords. The motor deficit scores in nebivolol group were different from I/R group at 72 h (3.25 0.70 vs. 1.75 +/- 1.28, p=0.01). I/R produced a significant increase in the superoxide dismutase (SOD), xanthine oxidase (XO), adenosine deaminase (ADA) and myeloperoxidase (MPO) activities in spinal cord tissue when compared with control group. Nebivolol treatment prevented the increase of all those enzymes activities produced by I/R. A significant decrease in spinal cord glutathione peroxidase (GSH-Px) level was seen in I/R group and nebivolol treatment prevented the decrement in the spinal cord tissue GSH-Px contents. On the other hand, I/R produced a significant increase in the spinal cord tissue malondialdehyde (MDA) and nitric oxide (NO) contents, this was prevented by nebivolol treatment. In conclusion, this study demonstrates a considerable neuroprotective effect of nebivolol on neurological, biochemical and histopathological status during periods of spinal cord I/R in rabbits. (C) 2004 Elsevier Inc. All rights reserved.Öğe Protective effects of caffeic acid phenethyl ester against experimental allergic encephalomyelitis-induced oxidative stress in rats(Elsevier Science Inc, 2004) Ilhan, A; Akyol, O; Gurel, A; Armutcu, F; Iraz, M; Oztas, EBecause oxidative damage has been known to be involved in inflammatory and autoimmune-mediated tissue destruction, modulation of oxygen free radical production represents a new approach to the treatment of inflammatory and autoimmune diseases. Central nervous system tissue is particularly vulnerable to oxidative damage, suggesting that oxidation plays an important role in the pathogenesis of multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE). Caffeic acid phenethyl ester (CAPE), an active component of honeybee propolis, has been determined to have antioxidant, anti-inflammatory, antiviral, and anticancer activities. We have previously reported that CAPE inhibits ischemia-reperfusion injury and oxidative stress in rabbit spinal cord tissue. The present study, therefore, examined effects of CAPE on oxidative tissue damage in EAE in rats. Treatment with CAPE significantly inhibited reactive oxygen species (ROS) production induced by EAE, and ameliorated clinical symptoms in rats. These results suggest that CAPE may exert its anti-inflammatory effect by inhibiting ROS production at the transcriptional level through the suppression of nuclear factor kappaB activation, and by directly inhibiting the catalytic activity of inducible nitric oxide synthase. (C) 2004 Elsevier Inc. All rights reserved.Öğe Protective role of ?-tocopherol and caffeic acid phenethyl ester on ischemia-reperfusion injury via nitric oxide and myeloperoxidase in rat kidneys(Elsevier, 2004) Gurel, A; Armutcu, F; Sahin, S; Sogut, S; Ozyurt, H; Gulec, M; Kutlu, NOBackground: The aim of this study was to determine the acute effects of antioxidant caffeic acid phenethyl ester (CAPE) and alpha-tocopherol (vitamin E) on nitric oxide (NO) production, neutrophil infiltration, and antioxidant enzyme activities on an in vivo model of renal ischemia-reperfusion injury. Methods: Rats were divided into five equal groups each consisting six rats: sham operation, ischemia, ischemia-reperfusion (I/R), I/R plus CAPE, and I/R plus vitamin E groups. CAPE or vitamin E was administered intraperitoneally before reperfusion. After experimental procedure, rats were sacrificed and both ipsilateral and contralateral kidneys were removed and prepared for NO concentrations, myeloperoxidase (MPO), catalase (CAT) and superoxide dismutase (SOD) activities. Results: Acute administration of vitamin E decreased NO concentrations in both ipsilateral and contralateral renal tissues compared to I/R group. SOD activity was increased in I/R and I/R + CAPE groups compared to sham operation group. The most prominent results were encountered in MPO activities, which did not change in contralateral kidneys in both ischemia and I/R groups. There was a significant decrease in ipsilateral MPO activity in ischemia group and a significant increase in I/R group compared to sham operation group. Pretreatment with intraperitoneal CAPE significantly diminished the tissue MPO activity indicating the prevention of the neutrophil sequestration into the kidney. Conclusion: There is a role for CAPE in attenuation in renal damage after I/R injury of the kidney, in part at least by inhibition of neutrophil sequestration. (C) 2003 Elsevier B.V. All rights reserved.Öğe Thoracic epidural anaesthesia and analgesia with bupivacaine for transsternal thymectomy for myasthenia gravis(Blackwell Science Ltd, 1997) Akpolat, N; Tilgen, H; Gursoy, F; Saydam, S; Gurel, AThe present study describes the management of a myasthenic patient undergoing transsternal thymectomy for whom thoracic epidural anaesthesia using 15 mt of bupivacaine 0.5% combined with isoflurane 0.4% and nitrous oxide in oxygen 50% provided good intra-operative relaxation followed by an uneventful recovery and eliminated the need for other post-operative analgesics.
