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    Protective Effects of Edaravone on Experimental Spinal Cord Injury in Rats
    (Karger, 2011) Ozgiray, Erkin; Serarslan, Yurdal; Ozturk, Oktay Hasan; Altas, Murat; Aras, Mustafa; Sogut, Sadik; Yurtseven, Taskin
    Background: Spinal cord injury (SCI) is a leading cause of morbidity and mortality among youth and adults. Secondary injury mechanisms within the spinal cord (SC) are well known to cause deterioration after an acute impact. Free radical scavengers are among the most studied agents in animal models of SCI. Edaravone is a scavenger of hydroxyl radicals. Methods: We aimed to measure and compare the effects of both methylprednisolone and edaravone on tissue and on serum concentrations of nitric oxide (NO), malondialdehyde (MDA) levels, superoxide dismutase (SOD) activity, glutathione peroxidase (GSH-Px) activity, and tissue total antioxidant capacity (TAC) in rats with SCI. SCI was induced in four groups of Wistar albino rats by a weight-drop method. The neurological function of the rats was periodically tested. At the end of the experiment, blood samples were collected, and SC tissue samples were harvested for biochemical evaluation. Results: The tissue level of NO was decreased in the edaravone-treated group compared with the no-treatment group (p < 0.05). The tissue levels of SOD and GSH-Px were higher in the edaravone-treated group than in the no-treatment group (p < 0.05). The serum levels of NO were lower in the edaravone-treated and methylprednisolone-treated groups than in the no-treatment group (p < 0.05). The serum levels of SOD in the edaravone-treated group did not differ from those of any other group. The serum levels of MDA in the edaravone-treated and no-treatment groups were higher than in the two other groups (p < 0.05). Tissue levels of MDA in the edaravone-treated group were lower than in the no-treatment group (p < 0.05). Tissue levels of TAC in the edaravone-treated group were higher than in the no-treatment and methylprednisolone-treated groups (p < 0.05). The neurological outcome scores of the animals in treatment groups did not depict any statistically significant improvement in motor functions. However, edaravone seemed to prevent further worsening of the immediate post-SCI neurological status. Conclusion: Our biochemical analyses indicate that edaravone is capable of blunting the increased oxidative stress that follows SCI. We show, for the first time, that edaravone enhances the TAC in SC tissue. This beneficial effect of edaravone on antioxidant status may act to minimize the secondary neurological damage that occurs during the acute phase after SCI. Copyright (C) 2012 S. Karger AG, Basel
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    Protective effects of minocycline on experimental spinal cord injury in rats
    (Elsevier Sci Ltd, 2015) Aras, Mustafa; Altas, Murat; Motor, Sedat; Dokuyucu, Recep; Yilmaz, Atilla; Ozgiray, Erkin; Seraslan, Yurdal
    Background: The effects of minocycline on neuronal injury after spinal cord injury (SCI) are limited and controversial. Therefore we aimed to investigate the protective effects of minocycline on tissue and on serum concentrations of malondialdehyde (MDA) levels, superoxide dismutase (SOD) activity, glutathione peroxidase (GSH-Px) activity, tissue total antioxidant and oxidant status (TAS and TOS, respectively), and AST and LDH levels in rats with SCI. Methods: This study was performed on 7-8 weeks 38 male Wistar albino rats. The animals were randomly divided into five groups: group 1, Sham (n = 8); group 2, SCI (spinal cord injury)/control (n = 8); group 3, SCI + minocycline3 (n = 7); group 4, SCI + minocycline30 (n = 8) and group 5 SCI + minocycline90 (n = 7). Blood and tissue samples were analysed for MDA, SOD, GSH-Px, TAS, TOS, AST and LDH levels. Results: The MDA levels were significantly higher in SCI group compared to sham group (p < 0.001), and MDA levels were also significantly higher in SCI group compared to SCI + M-3, SCI + M-30, SCI + M-90 (p < 0.05). SOD levels were significantly higher in SCI + M-30 when compared to SCI and SCI + M-3 groups (p < 0.05). GSH-Px levels decreased significantly in SCI and SCI + M-3 groups compared to sham (p < 0.05). SCI + M-3 group showed significantly decreased levels of TAS and TOS compared to SCI group (p < 0.05). TAS and TOS levels significantly increased in SCI + M-90 group compared to SCI + M-3 and SCI + M-30 groups (p < 0.05). Conclusions: The present study demonstrates the dose-dependent antioxidant activity of minocycline against spinal cord injury in rats. Minocycline administration increased antioxidant enzyme levels and improved total antioxidant status. (C) 2015 Elsevier Ltd. All rights reserved.
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    Protective effects of tadalafil on experimental spinal cord injury in rats
    (Elsevier Sci Ltd, 2010) Serarslan, Yurdal; Yonden, Zafer; Ozgiray, Erkin; Oktar, Sueleyman; Guven, Esref Oguz; Sogut, Sadik; Yilmaz, Nebi
    Tadalafil is a selective inhibitor of cyclic guanosine monophosphate (cGMP)-specific phosphodiesterase type 5 (PDE5). Nitric oxide (NO) functions as a retrograde neurotransmitter in the spinal cord, and postsynaptic structures respond to NO by producing cGMP. The concentrations of cGMP in the spinal cord are controlled by the actions of PDE. The aim of the study was to evaluate and compare the effects of the use of both methylprednisolone and tadalafil on serum and tissue concentrations of NO, malondialdehyde (MDA) levels, superoxide dismutase (SOD) activity, and tissue glutathione peroxidase (GSH-Px) activity in rats with spinal cord injury (SCI). SCI was induced in Wistar albino rats by dropping a 10 g rod from a 5.0 cm height at T8-10. The 28 rats were randomly divided into four equal groups: tadalafil, methylprednisolone, non-treatment and sham groups. Rats were neurologically tested at 24 hours after trauma. At the end of the experiment, blood samples were collected and spinal cord tissue samples were harvested for biochemical evaluation. The tissue level of NO was increased in the tadalafil group compared with the non-treatment and methylprednisolone groups (p < 0.05). The tissue levels of SOD and GSH-Px did not differ between the groups. Serum levels of NO were higher in the tadalafil group than in the non-treatment group (p < 0.05). The increase in serum SOD levels was greater in the tadalafil group than the methylprednisolone group. Serum MDA levels in the tadalafll and methylprednisolone groups tended to be lower than in the non-treatment group (p > 0.05). Tissue MDA levels in the taclalafil and methylprednisolone groups tended to be lower than in the non-treatment group and sham groups (p > 0.05). Although there was no difference in neurological outcome scores between the taclalafil, methylprednisolone and non-treatment groups (p > 0.05), the animals in the taclalafil and methylprednisolone groups tended to have better Scores than the non-treatment group. Thus, tadalafil appears to be beneficial in reducing the effects of injury to the spinal cord by increasing tissue levels of NO and serum activity of SOD. (C) 2009 Elsevier Ltd. All rights reserved.