Yazar "Kiris, T" seçeneğine göre listele
Listeleniyor 1 - 4 / 4
Sayfa Başına Sonuç
Sıralama seçenekleri
Öğe The effects of memantine on lipid peroxidation following closed-head trauma in rats(Springer, 2005) Özsüer, H; Görgülü, A; Kiris, T; Çobanoglu, SMemantine is an uncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist. Unlike other NMDA antagonists, it has been used clinically for years for the treatment of Parkinson's disease, spasticity, and dementia without serious side effects. We aimed to investigate the therapeutic efficacy of memantine on a closed head trauma model. A total of 132 adult male Sprague-Dawley rats were randomly divided into four groups: sham-operated, control (closed head trauma), sham-vehicle (closed head trauma + saline), treatment (closed head trauma + memantine, 10 mg/kg, i.p.). A cranial impact was delivered to the skull, just in front of the coronal suture, over the left hemisphere, from the height of 7 cm. Saline or memantine were applied 15 min after trauma. Rats were euthanased 0.5, 1, 2, 6, 24, 48 h after trauma. Brain tissue samples were taken 5 mm away from the left frontal pole and also from the corresponding point of the contralateral hemispheres. Malondialdehyde activity (MDA) was considered to reflect the degree of lipid peroxidation. The MDA levels continued to increase for the first 2 h after the injury, then started to decrease gradually. Memantine treatment significantly reduced lipid peroxidation levels in the treatment group compared with other groups (P < 0.01). The findings of the present study indicate that memantine provides beneficial effects after closed head trauma in rats.Öğe Protective effect of the N-methyl-D-aspartate receptor antagonists, MK-801 and CPP on cold-induced brain oedema(Springer Wien, 1999) Görgülü, A; Kiris, T; Ünal, F; Türkoglu, Ü; Küçük, M; Çobanoglu, SCold injury model in rat was used to determine the effect of treatment with the competitive NMDA antagonists CPP and the noncompetitive NMDA antagonist MK-801 in cerebral oedema. MK-801 was applied in doses of 1 mg/kg and CPP of 10 mg/kg, 15 min. after injury. Control animals received 1 mi saline at the same time interval after injury. Tissue samples from the core and periphery of the lesion of the injured hemisphere and from the symmetrical location of the undamaged contralateral hemisphere were removed 24 hours after injury. Blood brain barrier permeability, brain water content and tissue specific gravity values were determined. MK-801 was found beneficial for reducing the oedema and restore the blood brain barrier permeability at the penumbral zone of the lesion, whereas both MK-801 and CPP were found ineffective for prevention of oedema accumulation at the core of the lesion.Öğe Superoxide dismutase activity and the effect of N-methly-D-aspartate antagonists on lipid peroxidation in the early phase of cold injury(Springer, 1999) Kiris, T; Görgülü, A; Ünal, F; Türkoglu, Ü; Çobanoglu, S; Ekuklu, GFree radicals, lipid peroxidation and excitatory amino acids have been implicated in the secondary mechanisms of traumatic brain injury. We used the cold injury model in rats to assess the endogenous activity of the protective enzyme superoxide dismutase (SOD) and the lipid peroxidation level in the contused tissue at an early phase of injury. Furthermore, we treated the rats with two different N-methyl-D-aspartate receptor antagonists, namely MK-801 and CPP, and evaluated their effect on lipid peroxidation in the contused tissue. Rats were divided into four groups: sham, control, treatment 1 and treatment 2 groups (n = 16 for each group). Thirty and 60 min after craniectomy or injury, tissue samples were removed. SOD activity didn't change in this period. However, lipid peroxidation in terms of malondialdehyde (MDA) amount showed a significant increase at 60 min. Fifteen minutes after injury, MK-801 (1 mg/kg), CPP (10 mg/kg) or saline (1 ml) were applied intraperitoneally in treatment 1, treatment 2 and the control groups, Treatment with MK-801 attenuated MDA levels, whereas treatment with CPP did not. The protective effect of MK-801 achieved statistical significance. These results demonstrate that SOD activity does not change in the Parry period of cold injury. Moreover, these results show that lipid peroxidation increases after 60 min of cold injury, and treatment with MK-801 15 min after injury can prevent this elevation.Öğe Superoxide dismutase activity and the effects of NBQX and CPP on lipid peroxidation in experimental spinal cord injury(Springer Verlag, 2000) Görgülü, A; Kiris, T; Ünal, F; Turkoglu, Ü; Küçük, M; Çobanoglu, SThe endogenous activity of the neuroprotective enzyme superoxide dismutase (SOD) and the amount of lipid peroxidation in the early phase of experimental spinal cord injury, together with the effects of N-methyl-D-aspartate (NMDA) antagonist CPP and non-NMDA antagonist NBQX on lipid peroxidation were evaluated. The clip compression model was used for the production of a standardized spinal cord trauma. SOD activity and malondialdehyde (MDA) levels - as an indicator of lipid peroxidation - were determined in the injured segment of the spinal cord 30 and 60 min after injury. SOD activity did not change in this period, whereas MDA levels at 30 and 60 min after trauma were significantly elevated. Intrathecal administration of CPP or NBQX 15 min after injury produced statistically significant reductions in MDA elevation 60 min after injury. NBQX was found to be more effective than CPP. These results demonstrated that intrathecal local application of excitatory amino acid receptor antagonists can protect the spinal cord from secondary damage caused by the generation of lipid peroxides in experimental spinal cord injury.
