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    Effects of iloprost and piracetam in spinal cord ischemia-reperfusion injury in the rabbit
    (NATURE PUBLISHING GROUP, 2011) Kalkan, E.; Keskin, F.; Kaya, B.; Esen, H.; Tosun, M.; Kalkan, S. S.; Erdi, F.
    Study design: Experimental Study. Objectives: The aim of this study was to investigate the neuroprotective effects of iloprost and piracetam on spinal cord ischemia/reperfusion (I/R) injury in the rabbit. Settings: The Experimental Research Center of Selcuk University, Konya, Turkey. Methods: A total of 24 rabbits were divided into four groups of six rabbits each, as follows: group 1 (n = 6) sham, laparotomy only; group 2 (n = 6) I/R; group 3 (n = 6) I/R + iloprost; and group 4 (n = 6) I/R + piracetam. I/R was established in groups 2, 3 and 4. Subsequently, they were followed up neurologically for 24 h until the rabbits were killed; biochemical and histopathological examinations of samples from the spinal cord were carried out. Results: Neurological examination results were significantly better in the iloprost and piracetam groups compared with the I/R group (P<0.05). Neuroprotection was achieved with iloprost and piracetam by suppressing malondialdehyde (P<0.05), increasing glutathione peroxidase activity (P<0.05) and decreasing the xanthine oxidase level. In histopathological assessment, iloprost and piracetam groups were statistically different from the I/R group in terms of the number of apoptotic neurons in gray matter and white matter, as well as in terms of degenerated neurons and glial cells (P<0.05). No statistical difference was determined between the four groups in the number of degenerated glial cells (P>0.05). Conclusion: This study has shown that iloprost and piracetam have neuroprotective effects in I/R injury both neurologically and histopathologically because of inhibition of lipid peroxidation. Spinal Cord (2011) 49, 81-86; doi: 10.1038/sc.2010.76; published online 29 June 2010
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    The effects of prophylactic zinc and melatonin application on experimental spinal cord ischemia-reperfusion injury in rabbits: experimental study
    (NATURE PUBLISHING GROUP, 2007) Kalkan, E.; Çiçek, O.; Ünlü, Ali; Abuşoğlu, Sedat; Kalkan, S. S.; Avunduk, M. C.; Baysefer, A.
    Study design: Experimental study. Objectives: To determine the neuroprotective effects of zinc and melatonin on spinal cord ischemia-reperfusion (I/R) injuries of rabbits. Setting: The Experimental Research Centre of Selcuk University, Konya, Turkey. Methods: Twenty-four male rabbits underwent spinal cord ischemia by clamping the thoraco-abdominal aorta for 20 min. Twenty-minutes before the aortic clamping, animals received zinc, melatonin or a combination of both. Neurological examination of the animals was performed three times during reperfusion period. The animals were killed 24 h after reperfusion. Spinal cord samples were taken for biochemical and histopathological evaluation. Results: Pre-treated animals with zinc, melatonin or combination displayed better neurological outcomes than the I/R group (P < 0.05). Zinc, melatonin and combined treatment prevented spinal cord injury by reducing apoptosis rate (P < 0.05) and preserving intact ganglion cell numbers (P < 0.05). Zinc pre-treatment protected spinal cord by preventing malondialdehyde (MDA) formation (P = 0.002), increasing glutathione peroxidase (GPx) activity(P = 0.002) and decreasing xanthine oxidase enzyme activity (P = 0.026) at molecular level. Melatonin treatment also resulted with MDA formation (P = 0.002), increased GPx activity (P = 0.002) and decreased xanthine oxidase activity(P = 0.026). Conclusion: The results of the study showed that prophylactic zinc and melatonin use in spinal cord I/R not only suppressed lipid peroxidation by activating antioxidant systems but also had significant neuroprotective effects by specifically improving the neurological and histopathological situation.
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    Evaluation of TGF betal expression and comparison the thickness of different aorta layers in experimental diabetes
    (COMENIUS UNIV, 2011) Cuce, G.; Kalkan, S. S.; Esen, H. H.
    Background: It was aimed to investigate the effects of experimental diabetes on TGF beta 1 expression and tunica intima and media thickness in abdominal and thoracic aorta. Methods: Fourteen three months old female rats were divided into two groups, non-diabetic and streptozotocin (STZ) induced diabetic group. Hematoxylin-Eosin and Verhoeff's Van Gieson elastic staining and TGF beta 1 immunohistochemistry staining were performed. Abdominal and thoracic intima and media thickness of aortas were measured with the oculometer. Results: Evaluation of intima and media thickness measurements showed no significant statistical differences between non-diabetic and diabetic groups. TGF beta 1 expression increased significantly in thoracic diabetic (TD) group. Conclusion: The 60 day duration of diabetes is not sufficiently enough time for the development of pathological changes that could lead to thickening in aortic intima-media layers. TGF beta 1 expression was negative in the abdominal aorta that can predispose to the development of atherosclerosis, which could develop overtime. This finding may be interpreted as an appropriate basis for the development of atherosclerosis. In the thoracic aorta TGF beta 1 may coordinate cellular events such as tissue repair (Fig. 5, Ref. 23). Full Text in free PDF www.bmj.sk.