Person:
OKTAY, NİHAL ŞEHKAR

Profile Picture

Email Address

Birth Date

Research Projects

Organizational Units

OrgUnit Logo
Organizational Unit

Job Title

Last Name

OKTAY

First Name

NİHAL ŞEHKAR

Name

Filters

2016 - 20184
Reset filters

Settings

Subject: BLOOD ×

Search Results

Now showing 1 - 4 of 4
  • Thumbnail Image
    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.
  • Thumbnail Image
    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.
  • No Thumbnail Available
    PublicationMetadata only
    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.
  • No Thumbnail Available
    PublicationMetadata only
    Overpressure blast injury-induced oxidative stress and neuroinflammation response in rat frontal cortex and cerebellum
    (ELSEVIER SCIENCE BV, 2018) OKTAY, NİHAL ŞEHKAR; Toklu, Hale Z.; Yang, Zhihui; Oktay, Sehkar; Sakarya, Yasemin; Kirichenko, Nataliya; Matheny, Michael K.; Muller-Delp, Judy; Strang, Kevin; Scarpace, Philip J.; Wang, Kevin K. W.; Tumer, Nihal
    Background & aim: Overpressure blast-wave induced brain injury (OBI) and its long-term neurological outcome pose significant concerns for military personnel. Our aim is to investigate the mechanism of injury due to OBI. Methods: Rats were divided into 3 groups: (1) Control, (2) OBI (exposed 30 psi peak pressure, 2-2.5 ms), (3) Repeated OBI (r-OBI) (three exposures over one-week period). Lung and brain (cortex and cerebellum) tissues were collected at 24 h post injury. Results: The neurological examination score was worse in OBI and r-OBI (4.2 +/- 0.6 and 3.7 +/- 0.5, respectively) versus controls (0.7 +/- 0.2). A significant positive correlation between lung and brain edema was found. Malondialdehyde (index for lipid peroxidation), significantly increased in OBI and r-OBI groups in cortex (p < 0.05) and cerebellum (p < 0.01-0.001). The glutathione (endogenous antioxidant) level decreased in cortex (p < 0.01) and cerebellum (p < 0.05) of r-OBI group when compared with the controls. Myeloperoxidase activity indicating neutrophil infiltration, was significantly (p < 0.01-0.05) elevated in r-OBI. Additionally, tissue thromboplastin activity, a coagulation marker, was elevated, indicating a tendency to bleed. NGF and NF-kappa B proteins along with Iba-1 and GFAP immunoreactivity significantly augmented in the frontal cortex demonstrating microglial activation. Serum biomarkers of injury, NSE, TNF-alpha and leptin, were also elevated. Conclusion: OBI triggers both inflammation and oxidative injury in the brain. This data in conjunction with our previous observations suggests that OBI triggers a cascade of events beginning with impaired cerebral vascular function leading to ischemia and chronic neurological consequences.