Person: VELİOĞLU ÖĞÜNÇ, AYLİZ
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VELİOĞLU ÖĞÜNÇ
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AYLİZ
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Publication Open Access Protective Effect of Nigella Sativa Oil Against Indomethacin-Related Small Intestine and Gastric Mucosal Damage in Rats(AVES, 2021-04-26) VELİOĞLU ÖĞÜNÇ, AYLİZ; Gunay, Emre; Ozkan, Erkan; Abuoglu, Haci Hasan; Aykac, Asli; Ogunc, Ayliz Velioglu; Karanlik, Buse; Cetinel, Sule; Sehirli, Ahmet OzerBACKGROUND/AIMS The aim of this study was to investigate the effects of Nigella sativa (NS) oil form on reducing the damage caused by indomethacin in the stomach and duodenum of rats owing to their antioxidant and anti-inflammatory properties. MATERIAL and METHODS The rats were divided into 4 groups: group 1, saline-treated control group; group 2, NS-treated control group; group 3, saline-treated ulcer group and ulcers caused by indomethacin (30 mg/kg) and administration of physiological serum; group 4, NS-treated ulcer group, which is the group receiving NS oil after administration of indomethacin. At the end of the study, blood samples collected from animals were examined for tumor necrosis factor alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), and glutathione (GSH), malondialdehyde (MDA) levels and myeloperoxidase (MPO),and Na+/K+-ATPase activities in gastric and intestinal tissue samples. RESULTS Levels of TNF-alpha and IL-1 beta in serum and MDA and MPO values in tissue were found to be higher in the saline-treated ulcer group than in the saline-treated control group. In addition, tissue GSH and Na+/K+-ATPase levels were found to be lower. These values were found to be reversed when comparing NS-treated ulcer group to saline-treated ulcer group. Histopathological findings showed epithelial regeneration and improvement instead of dense tissue damage. CONCLUSION The strong antioxidant and anti-inflammatory effects of NS against potential small intestine and gastric damage were shown using an experimental indomethacin-induced ulcer model in rats. Hence, our study suggests that NS used together with indomethacin can prevent gastrointestinal damage; thus, this agent can create a new clinical therapeutic principle.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 Metadata only Meloxicam Exerts Neuroprotection on Spinal Cord Trauma in Rats(INFORMA HEALTHCARE, 2011) VELİOĞLU ÖĞÜNÇ, AYLİZ; Hakan, Tayfun; Toklu, Hale Zerrin; Biber, Necat; Celik, Hasan; Erzik, Can; Ogunc, Ayliz Velioglu; Cetinel, Sule; Sener, GokselTraumatic injury to the central nervous system results in the delayed dysfunction and neuronal death. Impaired mitochondrial function, generation of reactive oxygen species (ROS), and lipid peroxidation occur soon after traumatic spinal cord injury (SCI), while the activation of compensatory molecules that neutralize ROS occurs at later time points. The aim of the current study was to investigate the putative neuroprotective effect of the COX2 inhibitor meloxicam in a rat model of SCI. In order to induce SCI, a standard weight-drop method that induced a moderately severe injury (100 g/cm force) at T10, was used. Injured animals were given either 2 mg/kg meloxicam or saline 30 min postinjury by intraperitoneal injection. At seven days postinjury, neurological examination was performed and rats were decapitated. Spinal cord samples were taken for histological examination or determination of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity and DNA fragmentation. Formation of ROS in spinal cord tissue samples was monitored by using a chemiluminescence (CL) technique. SCI caused a significant decrease in spinal cord GSH content, which was accompanied with significant increases in CL, MDA levels, MPO activity, and DNA damage. On the other hand, meloxicam treatment reversed all these biochemical parameters as well as SCI-induced histopathological alterations. Furthermore, impairment of the neurological functions due to SCI was improved by meloxicam treatment. The present study suggests that meloxicam, reduces SCI-induced oxidative stress and exerts neuroprotection by inhibiting lipid peroxidation, GSH depletion, and DNA fragmentation.