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OKTAY, NİHAL ŞEHKAR

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NİHAL ŞEHKAR

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2015 - 20173
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Author: ALTURFAN, EBRU IŞIK × Subject: edaravone ×

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    Edaravone ameliorates the adverse effects of valproic acid toxicity in small intestine
    (SAGE PUBLICATIONS LTD, 2015) YARAT, AYŞEN; Oktay, S.; Alev, B.; Tunali, S.; Emekli-Alturfan, E.; Tunali-Akbay, T.; Koc-Ozturk, L.; Yanardag, R.; Yarat, A.
    Valproic acid (VPA) is a drug used for the treatment of epilepsy, bipolar psychiatric disorders, and migraine. Previous studies have reported an increased generation of reactive oxygen species and oxidative stress in the toxic mechanism of VPA. Edaravone, a free radical scavenger for clinical use, can quench free radical reaction by trapping a variety of free radical species. In this study, effect of edaravone on some small intestine biochemical parameters in VPA-induced toxicity was investigated. Thirty seven Sprague Dawley female rats were randomly divided into four groups. The groups include control group, edaravone (30 mg(-1) kg(-1) day(-1)) given group, VPA (0.5 g(-1) kg(-1) day(-1)) given group, VPA + edaravone (in same dose) given group. Edaravone and VPA were given intraperitoneally for 7 days. Biochemical parameters such as malondialdehyde, as an index of lipid peroxidation(LPO), sialic acid (SA), glutathione levels and glutathione peroxidase, glutathione-S-transferase, superoxide dismutase, catalase, myeloperoxidase, alkaline phosphatase (ALP), and tissue factor (TF) activities were determined in small intestine samples by colorimetric methods. Decreased small intestine antioxidant enzyme activities, increased LPO and SA levels, and increased activities of ALP and TF were detected in the VPA group. Based on our results edaravone may be suggested to reverse the oxidative stress and inflammation due to VPA-induced small intestine toxicity.
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    Investigation of the Effects of Edaravone on Valproic Acid Induced Tissue Damage in Pancreas
    (MARMARA UNIV, FAC PHARMACY, 2017-06-20) YARAT, AYŞEN; Oktay, Sehkar; Alev-Tuzuner, Burcin; Tunali, Sevim; Ak, Esin; Emekli-Alturfan, Ebru; Tunali-Akbay, Tugba; Koc-Ozturk, Leyla; Cetinel, Sule; Yanardag, Refiye; Yarat, Aysen
    Valproic acid (VPA), an effective antiepileptic and anticonvulsant drug, has some toxic side effects due to causing elevated oxidant production. The aim of this study is to investigate the effects of edaravone, a potent free radical scavenger on VPA induced toxicity and tissue damage by biochemical and histological examinations on pancreas. Female Sprague Dawley rats were divided into four groups as follows; control, edaravone, VPA, VPA+edaravon. VPA and edaravone were injected intraperitonally for seven days. Total protein, lipid peroxidation (LPO), sialic acid (SA) and glutathione (GSH) levels and alkaline phosphatase (ALP), tissue factor (TF), superoxide dismutase (SOD), glutathione-S-transferase GST), catalase (CAT), glutathione peroxidase (GPx) and myeloperoxidase (MPO) activities were determined in pancreas homogenates. In VPA given group, LPO and SA levels, and ALP, TF, MPO activities significantly increased and GST, CAT, GPx activities significantly decreased compared to control group. A marked morphological damage was detected in the VPA group. Ameliorative effects of edaravone were observed in SA, TF, CAT, GPx parameters and histological examination in the VPA group. Therefore, edaravone may be effective in moderation and/or reduction of toxic effects of VPA on pancreas.
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    PublicationOpen Access
    Edaravone Ameliorates Valproate-Induced Gingival Toxicity by Reducing Oxidative-Stress, Inflammation and Tissue Damage
    (MARMARA UNIV, FAC MEDICINE, 2016-05-10) YARAT, AYŞEN; Oktay, Sehkar; Alev, Burcin; Koc Ozturk, Leyla; Tunali, Sevim; Demirel, Sezin; Emekli Alturfan, Ebru; Tunali-Akbay, Tugba; Akyuz, Serap; Yanardag, Refiye; Yarat, Aysen
    Valproic acid (2-n-propylpentanoic acid, VPA), the most widely used antiepileptic drug, has potential adverse effects and it can disrupt the oxidant and antioxidant balance. Edaravone (3-methyl-1-phenyl-2-pyrazoline-5-one, EDA) is a potent free radical scavenger. In this study, the effect of EDA on gingiva in VPA induced toxicity was investigated. Female Sprague Dawley rats were randomly divided into four groups: control group, EDA (30 mg/kg/day) given group, VPA (0.5 g/kg/day) given group, and VPA+EDA (in same dose and time) given group. EDA and VPA were given intraperitoneally for seven days. Total protein, lipid peroxidation (LPO), sialic acid (SA) and reduced glutathione (GSH) levels and catalase (CAT), glutathione-S-transferase (GST), glutathione peroxidase (GPx), superoxide dismutase (SOD), myeloperoxidase (MPO), alkaline phosphatase (ALP), acid phosphatase (ACP), sodium potassium ATPase (Na+/K+-ATPase) and tissue factor (TF) activities were determined in gingiva homogenates. The VPA-induced increases were statistically significant for MPO (p<0.01), ACP (p<0.01), Na+/K+-ATPase (p<0.05) and TF (p<0.01) activities, but not for LPO level and ALP activities. EDA treatment markedly blunted all such elevated anomalies. Conclusively, VPA induced oxidative and inflammatory gingival tissue damage, reactions that were appreciably reversed by concurrent administration of EDA.