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  • Küçük Resim
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    Effects of memantine and clopidogrel alone and in combination in a cerebral ischemia-reperfusion model
    (Elsevier B.V., 2015) Özdemir, Hasan Hüseyin; İlhan, Selçuk; Demir, Caner Feyzi; Akgün, Bekir; Kapan, Oktay; Ataş, Eser; Berilgen, Muhammed Said
    There are many factors in cerebral ischemia that cause cell death. Glutamate receptor-mediated neurotoxicity is the major mechanism involved in hypoxic-ischemic brain injury (HIBI). Memantine is a low affinity, non-competitive NMDA antagonist blocker, while clopidogrel is an antiplatelet agent used in the treatment of ischemic stroke. The aim of this study is to investigate the effects of clopidogrel and memantine (alone and in combination) on HIBI. Thirty-five Sprague-Dawley rats were exposed to hypoxia for 10 min by ligation of the bilateral common carotid artery. Following this, the rats were divided equally into groups as follows: control, ischemia, memantine (IM), clopidogrel (IC) and memantine + clopidogrel (IMC). Drug therapy was administered for a period of five days, after which all rats were sacrificed and malondialdehyde (MDA), total antioxidant status (TAS), total oxidant (TOS) values, and oxidative stress index (OSI) were determined in brain tissue. MDA and TOS values were significantly higher in the group that underwent ischemia than in the control group. MDA, TOS and OSI values were significantly lower in the groups treated with IM, IC, or IMC than in the group that underwent ischemia. Although it was not significant, TOS and OSI were lower in the groups that underwent combined treatment than in the groups that underwent treatment with IM or IC alone. Our results indicate that memantine and clopidogrel treatment, when used individually, reduce oxidative stress in HIBH more so than when these treatments are combined. This may be due to potential pharmacokinetic mechanisms of the combined therapy.
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    Öğe
    Plasma Cytokine Levels in Migraineurs During and Outside of Attacks
    (Modestum Ltd, 2015) Aydin, Meliha; Demir, Caner Feyzi; Arikanoglu, Adalet; Bulut, Serpil; Ilhan, Nevin
    The hypothesis of cytokines as possible pain mediators in neurovascular inflammation offers a potential mechanism for the generation of migraine pain, but few studies examined cytokine levels in migraine patients. The aim of this study was to determine the levels of TNF-a, IL-4, IL-5, IL-6, IL-10, and IFN-gamma in serum of patients with migraine during attacks and attack-free periods. We evaluated 70 patients with migraine. Patients ranged in age from 17 to 55 19 healthy people without any diagnosis of migraine or headache were used as a control group. Levels of TNF-a, IL-4, IL-5, IL-6, IL-10, and IFN-gamma in plasma samples were determined by enzyme-linked immunosorbent assay (ELISA) techniques. The patients were classified as migraine with aura during attack, migraine with aura outside attack, migraine without aura during attack, migraine without aura outside attack according to migraine form presentation. TNF-a levels in migraine patients were significantly higher than in healthy controls. There was a significant change in serum TNF-a levels in patients with migraine with aura during migraine attacks. The levels of IL-6 high in all migraine subgroups compared to controls. In ictal groups, IL-10 levels were found higher than in interictal groups and healthy controls (p<0.05). Changes of the level of TNF-a, IL-6 and IL-10 in the blood of patients with migraine may suggest that neurogenic inflammation participates in the pathogenesis of migraine.