Person: VELİOĞLU ÖĞÜNÇ, AYLİZ
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VELİOĞLU ÖĞÜNÇ
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AYLİZ
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Publication Open Access Propylthiouracil-induced hypothyroidism protects ionizing radiation-induced multiple organ damage in rats(BIOSCIENTIFICA LTD, 2006-05) VELİOĞLU ÖĞÜNÇ, AYLİZ; Sener, G.; Kabasakal, L.; Atasoy, B. M.; Erzik, C.; Velioglu-Ogunc, A.; Cetinel, S.; Contuk, G.; Gedik, N.; Yegen, B. C.The objective of this study was to examine the potential radioprotective properties of propylthiouracil (PTU)-induced hypothyroidism against oxidative organ damage induced by irradiation. Sprague-Dawley rats were pre-treated with saline or PTU (10 mg/kg i.p.) for 15 days, and were then exposed to whole-body irradiation (800 cGy). A group of rats were decapitated at 6 h after exposure to irradiation, while another group was followed for 72 h after irradiation, during which saline or PTU injections were repeated once daily. Lung, liver, kidney and ileum samples were obtained for the determination of malondialdehyde (MDA; an index of lipid peroxidation) and glutathione (GSH, an antioxidant) levels, myeloperoxidase activity (MPO; an index of tissue neutrophil accumulation) and collagen contents, while oxidant-induced DNA fragmentation was evaluated in the ileal tissues. All tissues were also examined microscopically and assayed for the production of reactive oxidants using chemiluminescence (CL). Lactate dehydrogenase (LDH), an indicator of tissue damage, and turnout necrosis factor-alpha (TNF alpha) were assayed in serum samples. Irradiation caused a significant decrease in GSH level, which was accompanied by significant increases in MDA levels, MPO activity, CL levels and collagen content of the tissues studied (P < 0.05-0.001). Similarly, serum TNFa and LDH were elevated in the irradiated rats as compared with the control group. On the other hand, PTU treatment reversed all these biochemical indices, as well as histopathological alterations induced by irradiation. Our results suggested that PTU-induced hypothyroidism reduces oxidative damage in the lung, hepatic, renal and ileal tissues probably due to hypometabolism, which is associated with decreased production of reactive oxygen metabolites and enhancement of antioxidant mechanisms.Publication Metadata only Functional and structural changes of the urinary bladder following spinal cord injury; treatment with alpha lipoic acid(WILEY, 2017) VELİOĞLU ÖĞÜNÇ, AYLİZ; Ekiz, Arif; Ozdemir-Kumral, Zarife Nigar; Ersahin, Mehmet; Tugtepe, Halil; Ogunc, Ayliz Velioglu; Akakin, Dilek; Kiran, Demir; Ozsavci, Derya; Biber, Necat; Hakan, Tayfun; Yegen, Berrak C.; Sener, Goksel; Toklu, Hale Z.BACKGROUND & AIMAlpha lipoic acid (LA) was shown to exert neuroprotection in trauma-induced spinal cord injury (SCI), which is frequently associated with urinary bladder complaints in patients with SCI. Accordingly, the protective effects of LA on biochemical and histological changes in bladder as well as functional studies were assessed. METHODSWistar albino rats were divided as control, SCI, and LA (50mg/kg/day, ip) treated SCI groups (SCI+LA). The standard weight-drop (100g/cm force at T10) method was used to induce a moderately severe SCI. One week after the injury, neurological examination was performed and the rats were decapitated. Bladder samples were taken for histological examination, functional (isolated tissue bath) studies, and for the measurement of biochemical parameters (malondialdehyde, MDA; gluthathione, GSH; nerve growth factor, NGF; caspase-3, luminol and lucigenin chemiluminescences). RESULTSSCI caused a significant (P<0.001) increase in the detrusor muscle thickness. It increased the contractility responses to carbachol and relaxation responses to papaverine (P<0.05-0.001). There were also significant alterations in MDA, caspase-3, luminol, and lucigenin chemiluminescences with concomitant decreases in NGF and GSH (P<0.05). LA treatment reversed histological and functional (contraction and relaxation responses) changes induced by SCI (P<0.05-0.001), but no significant recovery was observed in the impaired neurological functions. CONCLUSIONThese results indicate that LA have a beneficial effect in improving the bladder tonus via its antioxidant and anti-inflammatory actions following SCI.Publication Metadata only Montelukast protects against renal ischemia/reperfusion injury in rats(ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD, 2006) VELİOĞLU ÖĞÜNÇ, AYLİZ; Sener, Goksel; Sehirli, Ozer; Velioglu-Ogunc, Ayliz; Cetinel, Sule; Gedik, Nursal; Caner, Metin; Sakarcan, Abdullah; Yegen, Berrak C.Background: Oxygen free radicals are important components involved in the pathophysiological processes observed during ischemia/reperfusion (I/R). Objective: This study was designed to assess the possible protective effect of montelukast, a selective antagonist of cysteinyl leukotriene receptor 1 (CysLT1), on renal VR injury. Methods: Wistar albino rats were unilaterally nephrectomized and subjected to 45 min of renal pedicle occlusion followed by 6 h of reperfusion. Montelukast (10 mg kg(-1), i.p.) or saline was administered at 15 min prior to ischemia and immediately before the reperfusion period. At the end of the reperfusion period, following decapitation, kidney samples were taken for histological examination or for determination of renal malondialdehyde (MDA), an end product of lipid peroxidation; glutathione (GSH), a key antioxidant; and myeloperoxidase (MPO) activity, an index of tissue neutrophil infiltration. Formation of reactive oxygen species in renal tissue samples was monitored by using chemiluminescence (CL) technique with luminol and lucigenin probes. Creatinine, blood urea nitrogen and lactate dehydrogenase (LDH) activity were measured in the serum samples, while leukotriene B-4, TNF-alpha, IL-beta, JL-6 and total antioxidant capacity (AOC) were assayed in plasma samples. Results: Ischemia/reperfusion caused a significant decrease in renal GSH and plasma AOC, which was accompanied with significant increases in MDA level, MPO activity, and CL levels of the renal tissue concomitant with increased levels of the pro-inflammatory mediators, LDH activity, creatinine and BUN. On the other hand, montelukast treatment reversed all these biochemical indices as well as histopathological alterations induced by I/R. Conclusions: CysLT I receptor antagonist montelukast reversed I/R-induced oxidant responses, improved microscopic damage and renal function. It seems likely that montelukast protects kidney tissue by inhibiting neutrophil infiltration, balancing oxidant-antioxidant status, and regulating the generation of inflammatory mediators. (c) 2006 Elsevier Ltd. All rights reserved.