Yazar "Cayli, Suleyman R." seçeneğine göre listele

Listeleniyor 1 - 2 / 2
  • Küçük Resim Yok
    Öğe
    Neuroprotective effect of etomidate on functional recovery in experimental spinal cord injury
    (Pergamon-Elsevier Science Ltd, 2006) Cayli, Suleyman R.; Ates, Ozkan; Karadag, Nese; Altinoz, Eyup; Yucel, Neslihan; Yologlu, Saim; Kocak, Ayhan
    Objective: Primary impact to the spinal cord causes rapid oxidative stress after injury. To protect neural tissue, it is important to prevent secondary pathophysiological mechanisms. Etomidate, a strong antiexcitotoxic agent, stimulates the gamma aminobutyric acid (GABA) receptors. The purpose of this study was to investigate neurobehavioral and histological recovery and to evaluate the biochemical responses to treatment of experimental spinal cord injury (SCI) in rats with etomidate or methylprednisolone (MP) or both etomidate and MP. Material and methods: Seventy-two rats were randomly allocated into six groups: a control group (laminectomy alone), a trauma group (laminectomy + trauma), a methylprednisolone group (30 mg/kg MP), an etomidate group (2 mg/kg), a methylprednisolone, and etomidate combined treatment group (30 mg/kg MP and 2 mg/kg etomidate) and a vehicle group. Six rats from each group were killed at the 24th hour after the injury. Malondialdehyde, glutathione, nitric oxide and xanthine oxidase levels were measured. Neurological functions of the remaining rats were recorded weekly. Six weeks after injury, all of those rats were killed for histopathological assesssment. Conclusion: Etomidate treatment immediately after spinal cord injury has similar neuroprotection to MR In spite of different neuroprotection mechanisms, combined treatment with MP and etomidate does not provide extra protection. (c) 2006 ISDN. Published by Elsevier Ltd. All rights reserved.
  • Küçük Resim Yok
    Öğe
    Neuroprotective effect of mexiletine in the central nervous system of diabetic rats
    (Springer, 2006) Ates, Ozkan; Cayli, Suleyman R.; Altinoz, Eyup; Yucel, Neslihan; Kocak, Ayhan; Tarim, Ozcan; Durak, Akif
    Both experimental and clinical studies suggests that oxidative stress plays an important role in the pathogenesis of diabetes mellitus type I and type 2. Hyperglycaemia leads to free radical generation and causes neural degeneration. In the present study we investigated the possible neuroprotective effect of mexiletine against streptozotocin-induced hyperglycaemia in the rat brain and spinal cord. 30 adult male Wistar rats were divided into three groups: control, diabetic, and diabetic-mexiletine treated group. Diabetes mellitus was induced by a single injection of streptozotocin (60 mg/kg body weight). Mexiletine (50 mg/kg) was injected intraperitoneally every day for six weeks. After 6 weeks the brain, brain stem and cervical spinal cord of the rats were removed and the hippocampus, cortex, cerebellum, brain stem and spinal cord were dissected for biochemical analysis (the level of Malondialdehide [MDA], Nitric Oxide [NO], Reduced Glutathione [GSH], and Xanthine Oxidase [XO] activity). MDA, XO and NO levels in the hippocampus, cortex, cerebellum, brain stem and spinal cord of the diabetic group increased significantly, when compared with control and mexiletine groups (P < 0.05). GSH levels in the hippocampus, cortex, cerebellum, brain stem and spinal cord of the diabetic group decreased significantly when compared with control and mexiletine groups (P < 0.05). This study demonstrates that mexiletine protects the neuronal tissue against the diabetic oxidative damage.