Time filter

Source Type

Yildirim Z.,Etimesgut Public Health Laboratory | Emmez H.,Gazi University | Kale A.,Gazi University
Oxidation Communications | Year: 2014

Radical oxygen species produced after injury counteracts antioxidant activity and frequently causes severe oxidative stress for the tissues. Alpha-lipoic acid (LA) is a powerful antioxidant. The aim of the study was to investigate the effects of LA supplementation on the levels of tumor necrosis factor-a (TNF-a), malondialdehyde (MDA), and total antioxidant status (TAS) in eye after spinal cord trauma. Twenty-four adults, male, New Zealand rabbits were divided into ischemia (n=8), control (n=8), and treatment groups (n=8). The abdominal aorta was clamped for 30 min by an aneurysm clip, approximately 1 cm below the renal artery and 1 cm above the iliac bifurcation in ischemia and treatment groups. In the control group, only laparotomy was performed. 25 cm3 of saline in control group and 100 mg/kg LA were administered intraperitoneally in the treatment group after closure of the incision. The animals were killed 48 h after the operation. Vitreous samples were collected for analysis. Vitreous levels of TNF-α, MDA, and TAS were analysed according to markers of oxidative stress and inflammation. The vitreous MDA and TNF-a levels were significantly higher in the ischemia group when compared to the control group (p<0.05). The vitreous MDA and TNF-α levels were significantly lower in the LA group when compared to the ischemia group (p<0.05). There was no significant difference between the vitreous TAS levels of the groups (p>0.05). Although further studies considering different dose regimens and time intervals are required, the results of the our study prove that LA acid has favourable effects on experimental spinal cord ischemia-reperfusion injury. Source

Yildirim Z.,Etimesgut Public Health Laboratory | Ucgun N.I.,Ankara Numune Education and Research Hospital | Yildirim F.,Duatepe Government Hospital | Sepici-Dincel A.,Gazi University
International Journal of Gerontology | Year: 2012

Background: Age-related macular degeneration (AMD) is the leading cause of irreversible visual impairment and blindness among persons aged 60 years and older. Although inflammation has been postulated to have a role in the pathogenesis of AMD, epidemiologic studies have not shown a relationship between systemic inflammation or presence of inflammatory markers at AMD. The aim of our study was to evaluate the differences in various types of cytokines and intracelluler signaling molecules for the onset and progression of AMD. Materials and methods: There were two groups in our study; Group 1, which acted as the control group (n = 30, mean age 67.60 ± 8.32 years), and Group 2, consisting of AMD patients (n = 22, mean age 70.10 ± 10.33 years). From serum samples, vascular endothelial growth factor (VEGF) (pg/mL), interleukin-6 (IL-6) and interleukin-1β (IL-1β) (pg/mL), nitrotyrosine (nmol/L) levels were determined by enzyme linked-immuno-sorbent assay method. Nitrite/Nitrate levels were measured by photometric method (μmol/L). Results: There were no significant differences between the groups with regard to age, VEGF, IL-1β, nitrite/nitrate, and nitrotyrosine. The significant result was the mean IL-6 levels that were higher in the AMD group (55.03 ± 60.03 pg/mL) than in the control group (16.08 ± 8.24 pg/mL, p < 0.001). Conclusion: IL-6 induces an ocular inflammatory response often accompanied by the breakdown of the blood-ocular barrier. The increased levels of IL-6 can support the hypothesis that AMD may be partially mediated through inflammatory mechanisms. © 2012, Taiwan Society of Geriatric Emergency & Critical Care Medicine. Published by Elsevier Taiwan LLC. All rights reserved. Source

Kurt G.,Gazi University | Yildirim Z.,Etimesgut Public Health Laboratory | Cemil B.,Fatih University | Celtikci E.,Gazi University | Kaplanoglu G.T.,Gazi University
Journal of Neurosurgery: Spine | Year: 2014

Object. The object of this study was to conduct a prospective, randomized, laboratory investigation of the neuroprotective effects of curcumin functionally, biochemically, and histologically in an experimental acute spinal cord ischemia-reperfusion injury on rabbits. Methods. Eighteen rabbits were randomly assigned to 1 of 3 groups: the sham group, the ischemia-reperfusion group, or the curcumin group. Spinal cord ischemia was induced by applying an infrarenal aortic cross-clamp for 30 minutes. At 48 hours after ischemia, neurological function was evaluated with modified Tarlov criteria. Biochemical changes in the spinal cord and plasma were observed by measuring levels of malondialdehyde (MDA), advanced oxidation protein products (AOPP), glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), nitrite/nitrate, and tumor necrosis factor-α (TNF-α). Histological changes were examined with H & E staining. Immunohistochemical staining with antibodies against caspase-3 was performed to evaluate cell apoptosis after ischemia. Results. In the curcumin group, neurological outcome scores were statistically significantly better compared with the ischemia-reperfusion group. In the ischemia-reperfusion group, MDA, AOPP, and nitrite/nitrate levels were significantly elevated in the spinal cord tissue and the plasma by the induction of ischemia-reperfusion. The curcumin treatment significantly prevented the ischemia-reperfusion-induced elevation of nitrite/nitrate and TNF-α. In addition, the spinal cord tissue and the plasma SOD, GSH, and CAT levels were found to be preserved in the curcumin group and not statistically different from those of the sham group. Histological evaluation of the tissues also demonstrated a decrease in axonal damage, neuronal degeneration, and glial cell infiltration after curcumin administration. Conclusions. Although further studies including different dose regimens and time intervals are required, curcumin could attenuate a spinal cord ischemia-reperfusion injury in rabbits via reducing oxidative products and proinflammatory cytokines, as well as increasing activities of antioxidant enzymes and preventing apoptotic cell death. ©AANS, 2014. Source

Yildirim Z.,Etimesgut Public Health Laboratory | Yildirim F.,Duatepe Government Hospital | Ucgun N.I.,Ankara Numune Education and Research Hospital | Sepici-Dincel A.,Gazi University
International Journal of Ophthalmology | Year: 2013

AIM: To examine them echanism of the development of pseudoexfoliation (PSX) syndrome via both cytokine formation and endothelial vasorelaxing and growth factors that will provide us new therapeutic insights for the treatment. METHODS: This is a cross sectional study included two groups; Group 1: control patients with nuclear cataract (n = 20, aged 51-80 years). Group 2: PSX patients with nuclear cataract (n = 18, aged 50-90 years). Patients with other ophthalmic problems and systemic diseases were excluded. Vascular endothelial grow th factor (VEGF), interleukin-6 (IL-6) and interleukin-1 β (IL-1 β) and nitroty rosine levels were determined through serum samples by Enzyme-linked immunosorbent assay (ELISA) method. Nitritenitrate levels were measured with photometric endpoint determination. RESULTS: There were no significant differences between the groups in terms of age, VEGF, IL-1 β, nitrite-nitrate and nitroty rosine. The significant results were the mean IL-6 levels that were higher in PSX group 2 (37.68 ± 29.52pg/mL) com pared to that in control group 1 (15.32 ± 10.08 pg/mL) (P < 0.001). CONCLUSION: Several interacting and extending biochemical pathways may lead to the promotion of VEGF and IL-6 expressions. IL-6 which is the only altered marker in our study may indirectly cause an increase of vascular permeability and neov ascularization. We suggest inflammation as a factor that can be involved in etiopathogenesis of PSX. Copyright International Journal of Ophthalmology Press. Source

Ucgun N.I.,Ankara Numune Education and Research Hospital | Yildirim Z.,Etimesgut Public Health Laboratory | Fikret C.Z.,Ankara Etlik Education and Research Hospital
Oxidation Communications | Year: 2011

In this study, the intraocular acetone levels in the vitreous fluid of diabetic patients and relation of acetone level to diabetic retinopathy have been investigated. The vitreous samples were obtained during vitrectomy for diabetic retinopathy in patients and for macular hole in controls. Acetone levels have been determined in 20 vitreous from 20 diabetic patients and 20 vitreous from 20 nondiabetic patients. The groups were matched for age and gender. Acetone levels were determined by a gas chromatography. The mean concentrations of acetone in vitreous fluid of diabetic patients (145.39±78.11 mg/dl) were significantly higher than that measured in control groups (23.94±13.92 mg/dl). Acetone levels occurred to a higher degree in diabetic vitreous than in nondiabetic vitreous. The correlation between diabetic retinopathy and acetone levels may indicate that acetone may play a role in diabetic retinopathy formation. This is the first study which is showing the elevated acetone levels in the vitreous of living diabetic patients. Source

Discover hidden collaborations