Publications by authors named "Dagci T"

Study Design: Pre-clinical animal experiment.

Objective: In this study, we investigated therapeutic effects of silibinin in a spinal cord injury (SCI) model. In SCI, loss of cells due to secondary damage mechanisms exceeds that caused by primary damage.

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Background: HCC is among the most common cancer. Ganoderma lucidum (G.lucidum) has been essential in preventing and treating cancer.

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N-methyl-D-aspartate (NMDA) receptor stimulation may lead to excitotoxicity, which triggers neuronal death in brain disorders. In addition to current clinical therapeutic approaches, treatment strategies by phytochemicals or their derivatives are under investigation for neurodegenerative diseases. In the present study, novel amino and 1,2,3-triazole derivatives of tomentosin were prepared and tested for their protective and anti-apoptotic effects in NMDA-induced excitotoxicity.

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The loss of neurons is strongly correlated with aging and aging-associated disorders. In this study, cell viability assays and mitochondrial function were performed to evaluate the effect of new spiro-pyrazole derivatives, prepared from aldehydes and 3-amino-1-phenyl-2-pyrazolin-5-one, on neuroprotection in an in vitro model of dopaminergic cell death induced by 1-methyl-4-phenylpyridinium (MPP). The percentages of neuroprotection by derivatives were found between 21.

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Purpose: The present study was conducted to determine oxidative stress and cell viability after contact with resin composites polymerized for different times.

Methods: Disk-shaped specimens of Admira Fusion, Ceram X One Universal, Solare x and Filtek Z550 (n = 12) were prepared, and two subgroups with polymerization times of 20 and 40 s were employed. The specimens were incubated with mouse fibroblast cells for 48 and 72 h, and changes in reactive oxygen species (ROS) production and cellular viability were determined by an assay with a cell-permeable fluorescent dye, 2',7'-dichlorodihydrofluorescein diacetate (HDCF-DA), and the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay, respectively.

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Neurodegenerative diseases affect millions of people. Major reasons behind the onset and progression of these diseases are still under investigation. Therefore, any approach that would treat/prevent progression is important.

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Recently, nuclear translocation and stability of nuclear factor erythroid 2 (NF-E2)-related factor 2 (Nrf2) have gained increasing attention in the prevention of oxidative stress. The present study was aimed to evaluate the regulatory role of glycogen synthase kinase-3β (GSK-3β) inhibition by tideglusib through the Nrf2 pathway in a cellular damage model. Gene silencing (siRNA-mediated) was performed to examine the responses of Nrf2-target genes (i.

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Objective: The aim of this in vitro study is to evaluate the effects of resveratrol (RES) addition on the cytotoxicity and microtensile bond strength (μTBS) of different adhesives.

Materials And Methods: Five self-etching adhesives (G-aenial Bond-GC, Optibond All in One-Kerr, Gluma Self Etch-Kulzer, Clearfil S Bond-Kuraray, and Nova Compo-B Plus-Imicryl) were tested. They were applied to L-929 cell culture by the extract method.

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Spinal cord injury (SCI) leads to vascular damage and disruption of blood-spinal cord barrier which participates in secondary nerve injury. Epidermal growth factor (EGF) is an endogenous protein which regulates cell proliferation, growth and differention. Previous studies reported that EGF exerts neuroprotective effect in spinal cord after SCI.

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Oxidative stress and apoptosis are both associated with various acute and chronic disorders. Thus, the aim of the present study is to synthesize imidazo[2,1-c][1,2,4]triazines derivatives and to evaluate their effects in HO-induced oxidative stress in human neuroblastoma cell line (SH-SY5Y cells). The effects of the compounds on cell viability were measured by MTT assay and the changes in stress and apoptosis-related proteins were investigated by PathScan Stress and Apoptosis Signaling Antibody Array kit and Western Blot technique.

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Study Design: Experimental animal study investigating the efficacy of C-terminal domain of tetanus toxin application as neuroprotective effects on rat brain in a model of spinal cord injury (SCI).

Objective: The aim of the present study was to investigate the possible role of C-terminal domain of tetanus toxin (Hc-TeTx) on cell death mechanisms including apoptosis and autophagy following SCI.

Summary Of Background Data: Traumatic SCI can lead to posttraumatic inflammation, oxidative stress, motor neuron apoptosis, necrosis, and autophagy of tissue.

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Neurodegenerative disorders including Alzheimer's disease, Parkinson's disease, and Huntington's disease affect millions of people in the world. Thus several new approaches to treat brain disorders are under development. The aim of the present study is to synthesize potential neuroprotective heterocyclic compounds based on pyrazolopyridine derivatives and then to evaluate their effects in MPP-induced neurodegeneration in human neuroblastoma cell line (SH-SY5Y cells).

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This study was designed to determine the in vivo performance of three different materials as scaffolds for dental pulp stem cells (DPSC) undergoing induced odontogenic differentiation. An odontogenic medium modified by the addition of recombinant human bone morphogenetic protein 2 was used in the experimental groups to induce differentiation. Mesenchymal stem cell medium was used in the control groups.

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Increased concentration of manganese (Mn) in the brain is known to be associated with excitotoxicity and neuroinflammation. Vinpocetine, an alkaloid derived from the plant Vinca minor L., basically shows its effect via phosphodiesterase inhibition and voltage-dependent Na channels.

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The aim of this study was to evaluate whether medium modification improves the odontogenic differentiation of human dental pulp stem cells (DPSC) in vitro and in vivo. DPSC isolated from human impacted third molar teeth were analysed for clusters of differentiation with flow cytometry. Odontogenic differentiation was stimulated by medium modification with the addition of bone morphogenetic protein 2 (BMP2).

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This study was designed to evaluate the cytotoxicity of four dentin bonding agents and the effects of an antioxidant addition. Group A: G-aenial Bond, Group B: Optibond All in One, Group C: Gluma Self Etch and Group D: Clearfil S(3) Bond were added to the medium using extract method. The cells were cultured with or without resveratrol (RES) addition.

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Background: N-methyl-d-aspartate (NMDA) receptors are major pharmacological targets to prevent or reduce the progression of neurodegenerative diseases. Successful therapy with NMDA receptor antagonists in humans has been limited by the severe side effects of complete receptor blockade. The aim of the present study was to investigate the possible protective effects of tideglusib against NMDA receptor overactivation in neural stem cells.

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Resveratrol, a natural phenolic compound, has been shown to prevent cardiovascular diseases and cancer and exhibit neuroprotective effects. In this study, we examined the neuroprotective and antioxidant effects of resveratrol against hydrogen peroxide in embryonic neural stem cells. Hydrogen peroxide treatment alone increased catalase and glutathione peroxidase activities but did not change superoxide dismutase levels compared with hydrogen peroxide + resveratrol treatment.

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Aims: Although hyperbaric oxygen (HBO) treatment following spinal cord injury (SCI) have been studied in terms of neurological function and tissue histology, there is a limited number studies on spinal cord tissue enzyme levels.

Main Methods: The effect of HBO treatment in SCI was investigated by measuring superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), nitric oxide synthase (NOS) and nitric oxide (NO) activity in the injured tissue. SCI was induced by applying an aneurysm clip extradurally at the level of T9-T11 vertebrae.

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CART mRNA and peptides are highly expressed in the anatomical structures composing the hypothalamo-pituitary-adrenal (HPA) axis and sympatho-adrenal system. Anatomical and functional studies suggest that CART peptides may have a role in the regulation of the neuroendocrine and autonomic responses during stress. Our previous study showed that CART peptides increased significantly in the male hypothalamus and amygdala 10min after the forced swim stress.

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Aims: The aim of this study is to determine the role of nitric oxide (NO) in neuropathic pain and the effect of embryonic neural stem cell (ENSC) transplantation on NO content in rat spinal cord neurons following spinal cord injury (SCI).

Main Methods: Ninety adult male Sprague-Dawley rats were divided into 3 groups (n=30, each): control (laminectomy), SCI (hemisection at T12-T13 segments) and SCI+ENSC. Each group was further divided into sub-groups (n=5 each) based on the treatment substance (L-NAME, 75 mg/kg/i.

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Introduction: Erectile dysfunction is common among patients with spinal cord injury (SCI).

Aim: This study aims to investigate the recovery of penile erectile functions of the rats with spinal cord injury (SCI) following transplantation of endogenous neuronal precursors cell (neuronal restricted precursors [NRP]/glial restricted precursors [GRP]) into the injured area of spinal cord.

Methods: Twenty-two rats were experimented in three groups.

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Purpose: We investigated functional recovery of the lower urinary system in rats with spinal cord injury after transplanting neuronal restricted precursors/glial restricted precursors or neural cells derived from bone marrow stromal cells into the injured area of the spinal cord.

Materials And Methods: A total of 30 rats underwent experimentation in 4 groups, including group 1--sham operation, group 2--spinal cord injury plus neuronal restricted precursor/glial restricted precursor transplantation, group 3--spinal cord injury plus bone marrow stromal cell transplantation and group 4--spinal cord injury control. All rats in the 4 groups were investigated urodynamically and sacrificed on day 28 after transplantation.

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The oxidative mechanisms of injury-induced damage of neurons within the spinal cord are not very well understood. We used a model of T8-T9 spinal cord injury (SCI) in the rat to induce neuronal degeneration. In this spinal cord injury model, unilateral avulsion of the spinal cord causes oxidative stress of neurons.

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