Person: VELİOĞLU ÖĞÜNÇ, AYLİZ
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VELİOĞLU ÖĞÜNÇ
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AYLİZ
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Publication Metadata only The role of cholinergic anti-inflammatory pathway in acetic acid-induced colonic inflammation in the rat(ELSEVIER IRELAND LTD, 2013) VELİOĞLU ÖĞÜNÇ, AYLİZ; Kolgazi, Meltem; Uslu, Unal; Yuksel, Meral; Velioglu-Ogunc, Ayliz; Ercan, Feriha; Alican, InciThe cholinergic anti-inflammatory pathway'' provides neurological modulation of cytokine synthesis to limit the magnitude of the immune response. This study aimed to evaluate the impact of the cholinergic anti-inflammatory pathway on the extent of tissue integrity, oxidant-antioxidant status and neutrophil infiltration to the inflamed organ in a rat model of acetic acid-induced colitis. Colitis was induced by intrarectal administration of 5% acetic acid (1 ml) to Sprague-Dawley rats (200-250 g; n = 7-8 per group). Control group received an equal volume of saline intrarectally. The rats were treated with either nicotine (1 mg/kg/day) or huperzine A (0.1 mg/kg/day) intraperitoneally for 3 days. After decapitation, the distal colon was scored macroscopically and microscopically. Tissue samples were used for the measurement of malondialdehyde (MDA) and glutathione (GSH) levels, and myeloperoxidase (MPO) activity. Formation of reactive oxygen species was monitored by using chemiluminescence (CL). Nuclear factor (NF)-kappa B expression was evaluated in colonic samples via immunohistochemical analysis. Trunk blood was collected for the assessment of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1 beta, IL-10, resistin and visfatin levels. Both nicotine and huperzine A reduced the extent of colonic lesions, increased colonic MDA level, high MPO activity and NF-kappa B expression in the colitis group. Elevation of serum IL-1 beta level due to colitis was also attenuated by both treatments. Additionally, huperzine A was effective to reverse colitis-induced high lucigenin-enhanced CL values and serum TNF-alpha levels. Colitis group revealed decreased serum visfatin levels compared to control group which was completely reversed by nicotine. In conclusion, modulation of the cholinergic system either by nicotine or ACh esterase inhibition improved acetic acid-induced colonic inflammation as confirmed by macroscopic and microscopic examination and biochemical assays. (C) 2013 Elsevier Ireland Ltd. All rights reserved.Publication Open Access Arginase activity and nitric oxide levels in patients with obstructive sleep apnea syndrome(2014-04-02) VELİOĞLU ÖĞÜNÇ, AYLİZ; Yuksel, M; Okur, Hk; Pelin, Z; Ogunc, Av; Ozturk, LPublication Open Access Protective effects of St. John's wort in the hepatic ischemia/reperfusion injury in rats(AVES, 2018-09-28) VELİOĞLU ÖĞÜNÇ, AYLİZ; Atalay, Suleyman; Soylu, Belkis; Aykac, Asli; Ogunc, Ayliz Velioglu; Cetinel, Sule; Ozkan, Naziye; Erzik, Can; Sehirli, Ahmet OzerObjectives: The purpose of this study was to investigate possible protective effects of St. John's wort in the hepatic ischemia/reperfusion injury. Material and Methods: The hepatic artery, portal vein, and bile duct were all clamped for 45 minutes to induce ischemia in rats, and after that reperfusion for 1 hour. SJW was administrated orally, once a day for 3 days before ischemia/reperfusion. The aspartate aminotransferase, alanine aminotransferase, tumor necrosis factor, and interleukin levels were measured in the serum samples. Luminol chemiluminescence, lucigenin luminol chemiluminescence levels; myeloperoxidase. The sodium-potassium ATPase (Na+/K+ ATPase) activity was determined in the liver tissue, and caspase-3 and caspase-9 activity with the bcl-2/bax ratio were measured by the western blot analysis. Results: The St. John's wort administration recovered the aspartate aminotransferase, alanine aminotransferase, tumor necrosis factor, and IL-1 beta levels serum parameters meaningfully, while ischemia/reperfusion caused an increase in luminol chemiluminescence, lucigenin luminol chemiluminescence, myeloperoxidase, caspase-3, and caspase-9 activity and led to a decrease in the B-cell lymphoma-2/bcl-2-associated X protein (bcl-2/bax) ratio and the Na+/K+ ATPase activity. Conclusion: The obtained results indicate protective effects of St. John's wort on the ischemia/reperfusion injury through various mechanisms, and we are able to suggest that St. John's wort can clinically create a new therapeutic principle.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 The Anti-Inflammatory and Neuroprotective Effects of Ghrelin in Subarachnoid Hemorrhage-Induced Oxidative Brain Damage in Rats(MARY ANN LIEBERT, INC, 2010) VELİOĞLU ÖĞÜNÇ, AYLİZ; Ersahin, Mehmet; Toklu, Hale Z.; Erzik, Can; Cetinel, Sule; Akakin, Dilek; Velioglu-Ogunc, Ayliz; Tetik, Sermin; Ozdemir, Zarife N.; Sener, Goeksel; Yegen, Berrak C.To elucidate the putative neuroprotective effects of ghrelin in subarachnoid hemorrhage (SAH)- induced brain injury, Wistar albino rats (n=54) were divided into sham-operated control, saline-treated SAH, and ghrelin-treated (10 mu g/kg/d IP) SAH groups. The rats were injected with blood (0.3mL) into the cisterna magna to induce SAH, and were sacrificed 48 h after the neurological examination scores were recorded. In plasma samples, neuron-specific enolase (NSE), S-100 beta protein, TNF-alpha, and IL-1 beta levels were evaluated, while forebrain tissue samples were taken for the measurement of malondialdehyde (MDA), glutathione (GSH), reactive oxygen species levels, myeloperoxidase (MPO), Na+-K+-ATPase activity, and DNA fragmentation ratio. Brain tissue samples containing the basilar arteries were obtained for histological examination, while cerebrum and cerebellum were removed for the measurement of blood-brain barrier (BBB) permeability and brain water content. The neurological scores were impaired at 48 h after SAH induction, and SAH caused significant decreases in brain GSH content and Na+-K+-ATPase activity, and increases in chemiluminescence, MDA levels, and MPO activity. Compared with the control group, the protein levels of NSE, S-100 beta, TNF-alpha, and IL-1 beta in plasma were also increased, while ghrelin treatment prevented all SAH-induced alterations observed both biochemically and histopathologically. The results demonstrate that ghrelin alleviates SAH-induced oxidative brain damage, and exerts neuroprotection by maintaining a balance in oxidant-antioxidant status, by inhibiting proinflammatory mediators, and preventing the depletion of endogenous antioxidants evoked by SAH.Publication Open Access Matrix Metalloproteinase-9 Level and Gene Polymorphism in Sleep Disordered Breathing Patients with or without Cardiovascular Disorders(AVES YAYINCILIK, 2013-03-05) VELİOĞLU ÖĞÜNÇ, AYLİZ; Yuksel, Meral; Kuzu-Okur, Hacer; Velioglu-Ogunc, Ayliz; Pelin, ZerrinObjective: Obstructive sleep apnea syndrome (OSAS) is associated with increased cardiovascular morbidity and mortality. We aimed to investigate the matrix metalloproteinase-9 (MMP-9) level and MMP-9 gene polymorphism in sleep apnea patients with or without cardiovascular disease. Study Design: Case-control study. Material and Methods: Two hundred nine patients [Mean age (+/- SD), 47 (+/- 12) yrs; M/F, 170/39] diagnosed with sleep-disordered breathing were included in the study. Serum MMP-9 level was performed using enzyme-linked immunosorbant assay (ELISA) and MMP-9 gene polymorphism with polymerase chain reaction-restriction fragment length polymorphism. We divided the patient group into two subgroups: (1) patients with confirmed cardiovascular disease, i.e. CV-P Group and (2) patients without cardiovascular disease, CV-N Group. We compared all parameters between the two groups. Results: There were 56 OSAS patients with cardiovascular disorder (CV-positive group) and 153 OSAS patients without cardiovascular disorder (CV-negative group). CC, CT and TT genotype distributions between groups were similar [31 (55%), 25 (45%), 0 (0%) vs 88 (57%), 61 (40%), 4 (3%); respectively, p>0.05]. MMP-9 level was significantly higher in CV-P patients (442.7 +/- 139.3 pg/mL) than in CV-N patients (364.4 +/- 165.0 pg/mL; p=0.0018). Conclusion: Our results showed that the presence of MMP-9 polymorphism was not associated with cardiovascular disease. MMP-9 level was higher in OSAS patients with cardiovascular disorders than without cardiovascular disorders. Finally, MMP-9 genotype was not associated with serum MMP-9 levels.Publication Metadata only Protective effects of spironolactone against hepatic ischemia/reperfusion injury in rats(TURKISH SURGICAL ASSOC, 2019) VELİOĞLU ÖĞÜNÇ, AYLİZ; Atalay, Suleyman; Soylu, Belkis; Aykac, Asli; Ogunc, Ayliz Velioglu; Cetinel, Sule; Ozkan, Naziye; Erzik, Can; Sehirli, Ahmet OzerObjective: In the present study, it was aimed to study the antioxidant effects of spironolactone (SPL) to determine its possible protective effects in hepatic ischemia reperfusion injury. Material and Methods: Hepatic artery, portal vein, and bile duct of Wistar albino rats were clamped for 45 minutes under anesthesia to form an ischemia period. Then reperfusion was allowed and the rats were decapitated 60 minutes later. SPL (20 mg/kg, p.o.) or SF was orally administered for 30 minutes before ischemia. Rats in the control arm underwent sham surgery and were administered isotonic saline. Liver function was studied by measuring aspartate aminotransferase (AST), alanine aminotransferase (ALT), tumor necrosis factor-alpha (TNF-alpha), and interleukin 1beta (IL-1 beta) levels. Malondialdehyde (MDA), glutathione (GSH), luminol, and lucigenin levels, myeloperoxidase (MPO) and Na+-K+- ATPase enzyme activities were analyzed to study tissue injury under light microscope. Results: While IR increased AST, ALT, TNF-alpha, and IL-1 beta levels and MDA, luminol, and lusigenin levels and MPO activities, it caused a decrease in GSH levels and Na+K+-ATPase activity. Spironolactone administration significantly improved these values. Conclusion: Protective effects of SPL against ischemia/reperfusion injury via various mechanisms suggest that this agent may become a novel treatment agent in clinical practice.Publication Open Access The protective effect of spironolactone and role of the Na+/K+-ATPase pump on intestinal ischemia/reperfusion injury(MARMARA UNIV, 2018-07-02) VELİOĞLU ÖĞÜNÇ, AYLİZ; Akyuz, Cebrail; Uzun, Orhan; Sunamak, Oguzhan; Velioglu-Ogunc, Ayliz; Cetinel, Sule; Sehirli, Ahmet OzerThe aim of this study was to evaluate the possible protective effect of spironolactone (SPL) and role of the Na-K ATPase pump on intestinal ischemia/reperfusion injury. In our study, the period of ischemia was established by clamping the mesenteric artery for 45 minunder anesthesia in Wistar albino rats and the animals left for reperfusion at the end of this period were decapitated after one hour. Spironolactone (20 mg kg(-1)) was administered orally for three days before ischemia, 30 minbefore ischemia. The control group rats were subjected to the Sham operation and administered saline solution. TNF-alpha and IL-1 beta levels were measured in the serum samples. Ileal Na+/K+-ATPase, myeloperoxidase (MPO) analysis were performed. Structural injury was assessed histopathologically. Ischemia/reperfusion increased serum TNF-alpha and IL-1 beta levels together with MPO activity, whereas these values were maintained at the control group levels through SPL activation. However, ischemia/reperfusion decreased Na+/K+-ATPase activity in ileal tissues; however, these parameters were found to be significantly increased with SPL activation. The protective effect of SPL against ischemia/reperfusion injury by different mechanisms, mainly the activity of the Na+/K+-ATPase pump, suggests that this nontoxic agent may constitute a new clinical therapeutic principle.Publication Metadata only Protective Potential of Montelukast Against Hepatic Ischemia/Reperfusion Injury in Rats(ACADEMIC PRESS INC ELSEVIER SCIENCE, 2010) VELİOĞLU ÖĞÜNÇ, AYLİZ; Oezkan, Erkan; Yardimci, Samet; Dulundu, Ender; Topaloglu, Uemit; Sehirli, Oezer; Ercan, Feriha; Velioglu-Oeguenc, Ayliz; Sener, GoekselIschemia and reperfusion (I/R) injury is characterized by significant oxidative stress, characteristic changes in the antioxidant system and organ injury leading to significant morbidity and mortality. This study was designed to assess the possible protective effect of montelukast, a selective antagonist of cysteinyl leukotriene receptor 1 (CysLT1), on hepatic I/R injury in rats. Wistar albino rats through clamping hepatic artery, portal vein, and bile duct, were subjected to 45 min of hepatic ischemia followed by 60 min reperfusion period. Montelukast (10 mg/kg; i.p.) was administered 15 min prior to ischemia and immediately before reperfusion period. At the end of the reperfusion period, the rats were killed by decapitation. Aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH) activity, and proinflammatory cytokines (TNF-alpha and IL-1 beta) were determined in blood samples. Malondialdehyde (MDA), and glutathione (GSH) levels and myeloperoxidase (MPO) and Na+, K+-ATPase activities were determined in the liver tissue samples while formation of reactive oxygen species was monitored by using chemiluminescence (CL) technique with luminol and lucigenin probes. Tissues were also analyzed histologically. Serum ALT, AST, and LDH activities were elevated in the I/R group, while this increase was significantly decreased by montelukast treatment. Hepatic GSH levels and Na+, K+- ATPase activity, significantly depressed by I/R, were elevated back to control levels in montelukast-treated I/R group. Furthermore, increases in tissue luminol and lucigenin CL, MDA levels, and MPO activity due to I/R injury were reduced back to control levels withPublication Metadata only The effect of phosphodiesterase-5 inhibition by sildenafil citrate on inflammation and apoptosis in rat experimental colitis(PERGAMON-ELSEVIER SCIENCE LTD, 2011) VELİOĞLU ÖĞÜNÇ, AYLİZ; Karakoyun, Berna; Uslu, Unal; Ercan, Feriha; Aydin, Mehmet Serif; Yuksel, Meral; Ogunc, Ayliz Velioglu; Alican, InciAims: To investigate the effect of sildenafil citrate (SIL) on the extent of tissue integrity, oxidant-antioxidant status and apoptosis in rats with colitis. Main methods: Colitis was induced by trinitrobenzenesulphonic acid (TNBS) in 40% ethanol (30 mg/ml; 0.8 ml) given intrarectally to Sprague-Dawley rats. Sildenafil (25 mg/kg/day) was administered after the induction of colitis and the treatment was continued for 7 days. Other groups received subcutaneously either N(G)-nitro- L-arginine methyl ester (L-NAME; 25 mg/kg) or N(G)-nitro-D-arginine methyl ester (D-NAME; 25 mg/kg) before SIL After decapitation, the distal colon was scored and stored for the measurement of malondialdehyde (MDA) level, glutathione (GSH) content, myeloperoxidase (MPO) activity and apoptosis. Oxidant generation was monitored by using chemiluminescence (CL). Blood was collected for tumor necrosis factor (TNF)-alpha and interleukin (IL)-10 assays. Key findings: The macroscopic lesion score of the colitis group was reduced by SIL (p<0.01) and this effect was abolished by L-NAME (p<0.01). Increase in colonic MDA along with a concomitant decrease in GSH of the colitis group was reversed by SIL (p<0.01 and p<0.001, respectively). L-NAME prevented the effect of SIL on GSH content (p<0.001). Sildenafil also reduced the elevated MPO of the colitis group (p<0.001) and this effect was reversed by L-NAME (p<0.01). Increase in lucigenin CL and serum TNF-alpha levels in the colitis group were also prevented by SIL (p<0.001 and p<0.01, respectively). Significance: Sildenafil is beneficial in TNBS-induced rat colitis partially by nitric oxide-dependent mechanisms via the maintenance of oxidant-antioxidant status, prevention of apoptosis, superoxide production and cytokine release. (C) 2011 Elsevier Inc. All rights reserved.