Person:
OKTAY, NİHAL ŞEHKAR

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OKTAY

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NİHAL ŞEHKAR

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  • PublicationOpen Access
    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.
  • Publication
    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.