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OKTAY, NİHAL ŞEHKAR

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NİHAL ŞEHKAR

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2016 - 20182
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Author: AKBAY, TUĞBA × Subject: BLOOD ×

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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.
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    Melatonin improves hyperglycemia induced damages in rat brain
    (WILEY, 2018) YARAT, AYŞEN; Gurel-Gokmen, Begum; Ipekci, Hazal; Oktay, Sehkar; Alev, Burcin; Ustundag, Unsal Veli; Ak, Esin; Akakin, Dilek; Sener, Goksel; Emekli-Alturfan, Ebru; Yarat, Aysen; Tunali-Akbay, Tugba
    Background Diabetes mellitus is an endocrine disorder which is characterized by the development of resistance to the cellular activity of insulin or inadequate insulin production. It leads to hyperglycemia, prolonged inflammation, and oxidative stress. Oxidative stress is assumed to play an important role in the development of diabetic complications. Melatonin is the hormone that interacts with insulin in diabetes. Therefore, in this study, the effects of melatonin treatment with or without insulin were examined in diabetic rat brain. Methods Results Rats were divided into five groups as control, diabetes, diabetes + insulin, diabetes + melatonin, and diabetes + melatonin + insulin. Experimental diabetes was induced by streptozotocin (60 mg/kg, i.p.). Twelve weeks after diabetes induction, rats were decapitated. Malondialdehyde, glutathione, sialic acid and nitric oxide levels, superoxide dismutase, catalase, glutathione-S-transferase, myeloperoxidase, and tissue factor activities were determined in brain tissue. Melatonin alone showed its antioxidant effect by increasing brain glutathione level, superoxide dismutase, catalase, and glutathione-S-transferase activities and decreasing malondialdehyde level in experimental diabetes. Although insulin did not have a significant effect on glutathione and glutathione-S-transferase, its effects on lipid peroxidation, superoxide dismutase, and catalase were similar to melatonin; insulin also decreased myolopeoxidase activity and increased tissue factor activity. Combined melatonin and insulin treatment mimicked the effects of insulin. Conclusion Addition of melatonin to the insulin treatment did not change the effects of insulin, but the detailed role of melatonin alone in the treatment of diabetes merits further experimental and clinical investigation.