Person: ŞENER, GÖKSEL
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ŞENER
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GÖKSEL
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Publication Metadata only Apocynin attenuates testicular ischemia-reperfusion injury in rats(W B SAUNDERS CO-ELSEVIER INC, 2015) ŞİMŞEK, FERRUH; Sener, T. Emre; Yuksel, Meral; Ozyilmaz-Yay, Nagehan; Ercan, Feriha; Akbal, Cem; Simsek, Ferruh; Sener, GokselObjective: This study was designed to examine the possible protective effect of apocynin, a NADPH oxidase inhibitor, against torsion/detorsion (T/D) induced ischemia/reperfusion (I/R) injury in testis. Methods: Male Wistar albino rats were divided into sham-operated control, and either vehicle, apocynin 20 mg/kg-or apocynin 50 mg/kg-treated T/D groups. In order to induce I/R injury, left testis was rotated 720 degrees clockwise for 4 hours (torsion) and then allowed reperfusion (detorsion) for 4 hours. Left orchiectomy was done for the measurement of tissue malondialdehyde (MDA), glutathione (GSH) levels, myeloperoxidase (MPO) activity, and luminol, lucigenin, nitric oxide (NO) and peroxynitrite chemiluminescences (CL). Testicular morphology was examined by light microscopy. Results: I/R caused significant increases in tissue luminol, lucigenin, nitric oxide and peroxynitrite CL demonstrating increased reactive oxygen and nitrogen metabolites. As a result of increased oxidative stress tissue MPO activity, MDA levels were increased and antioxidant GSH was decreased. On the other hand, apocynin treatment reversed all these biochemical indices, as well as histopathological alterations that were induced by I/R. According to data, although lower dose of apocynin tended to reverse the biochemical parameters, high dose of apocynin provides better protection since values were closer to the control levels. Conclusion: Findings of the present study suggest that NADPH oxidase inhibitor apocynin by inhibiting free radical generation and increasing antioxidant defense exerts protective effects on testicular tissues against I/R. The protection with apocynin was more pronounced with high dose. (C) 2015 Elsevier Inc. All rights reserved.Publication Metadata only Protective effects of Ginkgo biloba against acetaminophen-induced toxicity in mice(SPRINGER, 2006) ERCAN, FERİHA; Sener, G; Omurtag, GZ; Sehirli, O; Tozan, A; Yuksel, M; Ercan, F; Gedik, NBackground: The analgesic acetaminophen (AAP) causes a potentially fatal, hepatic centrilobular necrosis when taken in overdose. It was reported that these toxic effects of AAP are due to oxidative reactions that take place during its metabolism. Objective: In this study, we aimed to investigate the possible beneficial effect of Ginkgo biloba (EGb), an antioxidant agent, against AAP toxicity in mice. Methods: Balb/c mice were injected i.p. with: (1) vehicle, control (C) group; (2) a single dose of 50 mg/kg Ginkgo biloba extract, EGb group; (3) a single dose of 900 mg/kg i.p. acetaminophen, AAP group, and (4) EGb, in a dose of 50 mg/kg after AAP injection, AAP + EGb group. Serum ALT, AST, and tumor necrosis factor-alpha (TNF-alpha) levels in blood and glutathione (GSH), malondialdehyde (MDA) levels, myeloperoxidase (MPO) activity, and collagen contents in liver tissues were measured. Formation of reactive oxygen species in hepatic tissue samples was monitored by using chemiluminescence (CL) technique with luminol and lusigenin probe. Tissues were also examined microscopically. Results: ALT, AST levels, and TNF-alpha were increased significantly (p < 0.001) after AAP treatment, and reduced with EGb. Acetaminophen caused a significant (p < 0.05-0.001) decrease in GSH levels while MDA levels and MPO activity were increased (p < 0.001) in liver tissues. These changes were reversed by EGb treatment. Furthermore, luminol and lusigenin CL levels in the AAP group increased dramatically compared to control and reduced by EGb treatment (p < 0.01). Conclusion: Our results implicate that AAP causes oxidative damage in hepatic tissues and Ginkgo biloba extract, by its antioxidant effects protects the tissues. Therefore, its therapeutic role as a tissue injury-limiting agent must be further elucidated in drug-induced oxidative damage.Publication Metadata only Taurine protects against methotrexate-induced toxicity and inhibits leukocyte death(ACADEMIC PRESS INC ELSEVIER SCIENCE, 2005) YEGEN, BERRAK; Cetiner, M; Sener, G; Sehirli, AO; Eksioglu-Demiralp, E; Ercan, F; Sirvanci, S; Gedik, N; Akpulat, S; Tecimer, T; Yegen, BCThe efficacy of methotrexate (MTX), a widely used cytotoxic chemotherapeutic agent, is often limited by severe side effects and toxic sequelae. Regarding the mechanisms of these side effects, several hypotheses have been put forward, among which oxidative stress is noticeable. The present study was undertaken to determine whether taurine, a potent free radical scavenger, could ameliorate MTX-induced oxidative injury and modulate immune response. Following a single dose of methotrexate (20 mg/kg), either saline or taurine (50 mg/kg) was administered for 5 days. After decapitation of the rats, trunk blood was obtained and the ileum, liver, and kidney were removed to measure malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity, and collagen content, as well as histological examination. Our results showed that MTX administration increased the MDA, MPO activity, and collagen contents and decreased GSH levels in all tissues (P < 0.001), while these alterations were reversed in taurine-treated group (P < 0.05-0.01). Elevated (P < 0.001) TNF-alpha level observed following MTX treatment was depressed with taurine (P < 0.01). Oxidative burst of neutrophils stimulated by phorbol myristate acetate was reduced in saline-treated MTX group (P < 0.001), while taurine abolished this effect. Similarly, flow cytometric measurements revealed that leukocyte apoptosis and cell death were increased in MTX-treated animals, while taurine reversed these effects (P < 0.05). Reduced cellularity in bone marrow samples of MTX-treated group (P < 0.01) was reversed back to control levels in taurine-treated rats. Severe degeneration of the intestinal mucosa, liver parenchyma, glomerular, and tubular epithelium observed in saline-treated group was improved by taurine treatment. In conclusion, it appears that taurine protects against methotrexate-induced oxidant organ injury and inhibits leukocyte apoptosis and may be of therapeutic potential in alleviating the systemic side effects of chemotherapeutics. (c) 2005 Published by Elsevier Inc.Publication Metadata only Amelioration of sepsis-induced hepatic and ileal injury in rats by the leukotriene receptor blocker montelukast(CHURCHILL LIVINGSTONE, 2005) YEGEN, BERRAK; Sener, G; Sehirli, O; Cetinel, S; Ercan, F; Yuksel, M; Gedik, N; Yegen, BCBackground. Sepsis is a generalized inflammatory response, which involves organ systems remote from the locus of the initial infectious insult, involves the release of cytokines and the subsequent formation of reactive oxygen and nitrogen species. Objective: The aim of this study was to investigate the possible protective effect of montelukast, a leukotriene receptor blocker, against oxidative damage in the liver and ileum of septic rats. Methods: Sepsis was induced by cecal ligation and puncture method in female Wistar albino rats. Sepsis and sham operated (control) groups received either saline or montelukast (10 mg/kg, ip) immediately after the operation and at 12 h. Twenty-four hours after the surgery, rats were decapitated and malondialdehyde (MDA) content-an index of lipid peroxidation, glutathione (GSH) levels-a key antioxidant, myeloperoxidase (MPO) activity-an index of neutrophil infiltration, and collagen contents were determined in the liver and ileum. Formation of reactive oxygen species in liver and ileal tissue samples was monitored by using chemiluminescence (CL) technique with luminol and lucigenin probes. Both tissues were also analyzed histologically. Serum lactate dehydrogenase (LDH) and tumor necrosis factor-alpha (TNF-alpha) level were assessed in trunk blood. Results: Sepsis resulted in decreased GSH levels, and increased MDA levels, MPO activity, CL levels and collagen contents in both the liver and the ileum (P < 0.05 - P < 0.001) indicating the presence of the oxidative damage. Similarly, serum TNF-alpha and LDH were elevated in the sepsis group as compared to control group. On the other hand, montelukast treatment reversed all these biochemical indices, as well as histopathological alterations, which were induced by sepsis. Conclusion: Findings of the present study suggest that montelukast possesses an anti-inflammatory effect on sepsis-induced hepatic and intestinal damage and protects against oxidative injury by a neutrophil-dependent mechanism. (C) 2005 Elsevier Ltd. All rights reserved.Publication Open Access The effect of Cotinus coggygria L. ethanol extract in the treatment of burn wounds(2022-01-01) OKUYAN, BETÜL; ŞEN, ALİ; ŞENER, GÖKSEL; ERCAN, FERİHA; Erta B., OKUYAN B., ŞEN A., ERCAN F., Onel H., GÖGER F., Sener G.The overall aim of the present research is to evaluate for the first time the curative effect of Cotinus coggygria leaves on burn injury in an experimental burn model along with its anti-inflammatory and antioxidant activity potential. Also, phenolic compounds of C. coggygria were characterised by LC-MS/MS. Wistar albino rats weighing 200-250 g were exposed to 90 degrees C bath for 10 s to induce burn injury, involving 30% of the total body surface area. In the treatment groups, 5% C. coggygria ethanol extract was applied topically as a cream immediately after the burn. Blood and skin tissue samples were taken after decapitation at the 4th and 48th hours following the burn procedure. Interleukin 1-beta (IL-1 beta) and tumour necrosis factor (TNF-alpha) were determined in serum samples, and hydroxyproline, prostoglandin E2 (PGE2), and myeloperoxidase (MPO) activity and 8-hydroxy-2\"-deoxy-guanosine (8-OHdG) levels were determined in skin tissue samples. Increased levels of serum cytokines were decreased with C. coggygria treatment in both periods. MPO activity, prostaglandine (PGE2), and 8-OhdG levels increased, while hydroxyproline levels decreased due to burn damage. On the other hand, these parameters were returned to its normal levels with C. coggygria treatment. In addition, the tissue histology of animals treated with C. coggygria showed a complete epithelialization with increased collagenation. As a result, C. coggygria may be an alternative treatment approach for burns-induced skin damage and wounds.Publication Open Access The Influence of N-Acetylcysteine Alone and in Combination with Angiotensin Converting Enzyme Inhibitor and Angiotensin Receptor Antagonist on Systemic and Tissue Levels in Rats with Experimentally-Induced Chronic Renal Failure(ZOOLOGICAL SOC PAKISTAN, 2020) VELİOĞLU ÖĞÜNÇ, AYLİZ; Sehirli, Ahmet Ozer; Sayiner, Serkan; Velioglu-Ogunc, Ayliz; Serakinci, Nedime; Eksioglu-Demiralp, Emel; Yegen, Berrak; Ercan, Feriha; Sener, GokselThe protective effects of ACE inhibitor, Captopril, and angiotensin receptor blocker, Valsartan, were evaluated in the treatment of chronic renal failure (CRF) with and without the presence of N-acetylcysteine (NAC). The renal mass of Wistar albino rats was reduced at a rate of 5/6. Captopril, Valsartan and NAC were applied intra-peritoneal alone or in combination. Blood pressure and heart rate were monitored at weekly intervals over a period of six weeks. Serum creatinine, blood urea nitrogen (BUN), lactate dehydrogenase (LDH) activity, cytokines (TNF-alpha, IL-1 beta, IL-6) concentrations, urinary volume, creatinine, and both serum and urinary electrolyte levels were measured. In addition, the apoptosis rate of white blood cells was analysed from plasma samples. Tissue samples from the brain, heart, aorta and kidneys were used for analysis of the collagen content besides tissue luminol, lucigenin, malondialdehyde (MDA) and glutathione (GSH) levels. A significant difference was determined between the CRF group and the control group with regard to heart rate, blood pressure, serum creatinine, BUN, LDH, cytokines and urinary electrolyte levels. Furthermore, monocyte and neutrophil apoptosis, tissue luminol, lucigenin, malondialdehyde and collagen levels were found to increase. Tissue glutathione levels were found to decrease indicating oxidative damage. These results indicate that oxidative mechanisms induce tissue damage in CRF, and the angiotensin receptor blocker, Valsartan, improved oxidative tissue damage when used in combination with the ACE inhibitor, Captopril or NAC, yielded better results and could be a novel approach for the treatment of CRF when used in combination with anti-oxidants.Publication Metadata only Role of melatonin in reducing water avoidance stress-induced degeneration of the liver(SPRINGER, 2005) ERCAN, FERİHA; Contuk, G; Ercan, F; Cetinel, S; Cikler, E; Sener, GMelatonin, a pineal secretory product, is a potent scavenger of a variety of free radicals. We investigated the role of melatonin on water avoidance stress (WAS)-induced degenerations of the liver parenchyme. Wistar albino rats were exposed to acute WAS (aWAS group) or chronic WAS (cWAS group). Before exposing animals to acute (aWAS + mel group) or chronic WAS (cWAS + mel group), 10 mg/kg melatonin was injected i.p. The liver samples were investigated under light and transmission electron microscope. Malondialdehyde (MDA) and glutathione (GSH) levels were also determined. Prominent vascular congestion and dilated sinusoids, activated Kupffer cells with prominent morphology, dilated granular endoplasmic reticulum membranes, and focal picnotic nuclei were observed in the aWAS group; these morphological changes were severe in the cWAS group. MDA level was increased and GSH level was decreased significantly in the cWAS group. The morphology of liver parenchme in both the aWAS + mel and the cWAS + mel group showed that melatonin significantly reduced the degeneration in liver; besides, a significant decrease in MDA and an increase in GSH levels were observed in the cWAS + mel group. Based on the results, melatonin treatment significantly prevented WAS-induced morphological and biochemical changes in liver parenchyma.Publication Metadata only Protective effects of exercise on heart and aorta in high-fat diet-induced obese rats(CHURCHILL LIVINGSTONE, 2019) ERCAN, FERİHA; Elmas, Merve Acikel; Cakici, Seyit Enes; Dur, Ismail Rahmi; Kozluca, Ibrahim; Arinc, Melih; Binbuga, Berkant; Ozakpinar, Ozlem Bingol; Kolgazi, Meltem; Sener, Goksel; Ercan, FerihaWe investigated the protective effects of swimming exercise on high-fat diet-induced heart and aorta damage by evaluating oxidative stress and the endothelial nitric oxide (NO) system. Sprague Dawley rats were fed either standard chow (STD, 6% fat) or high-fat diet (HFD; 45% fat) for 18 weeks, with half of the animals trained by daily swimming sessions (EXC; 1 h per day for 5 days/week) for the last 6 weeks of the experimental period and half kept sedentary (SED). Heart and aorta tissues were prepared for routine light and electron microscopy evaluation. Endothelial NOS (eNOS) and inducible NOS (iNOS) distribution in the tissue samples were examined by immunohistochemistry. Biochemical examinations, including blood serum lipid profiles, malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), and tissue NO levels were measured. Deteriorated heart and aorta morphology, increased MDA levels and iNOS-immunoreactivity (iNOS-ir), as well as decreased GSH, NO, SOD, and eNOS-ir parameters were observed in the HFD+ SED group. These morphological and biochemical parameters were ameliorated in the HFD+ EXC group. Our study revealed that obesity-induced iNOS activation and increased oxidative stress in cardiac and aorta tissues. Exercise protected the obesity-induced cardiac and aortic tissue damage by modulating oxidant/antioxidant balance via involvement of the NO system.Publication Metadata only Protective Effects of Lycopene on Cerulein-Induced Experimental Acute Pancreatitis in Rats(ACADEMIC PRESS INC ELSEVIER SCIENCE, 2012) DULUNDU, ENDER; Ozkan, Erkan; Akyuz, Cebrail; Dulundu, Ender; Topaloglu, Umit; Sehirli, Ahmet Ozer; Ercan, Feriha; Sener, GokselBackground. The purpose of our study was to evaluate the protective effect of the strong antioxidant and anti-inflammatory agent, lycopene, on oxidative stress in a rat model of cerulein-induced acute edematous pancreatitis. Methods. Sprague-Dawley rats were pretreated with lycopene (50 mg/kg, i.p.) or saline 15 min before cerulein was given 20 mu g/kg (i.p.) at 1-h intervals within 4 h. Twelve hours after cerulein or saline injections, the animals were killed by decapitation. Blood samples were collected to analyze amylase, lipase, and proinflammatory cytokines (TNF-alpha and IL-1 beta). Pancreatic tissues were taken for the determination of tissue glutathione (GSH) and malondialdehyde (MDA) levels, Na+/K+-ATPase, and myeloperoxidase (MPO) activities. Tissue samples were also examined histologically. Results. Acute pancreatitis caused significant decrease in tissue GSH levels and Na+/K+-ATPase activity, while pancreatic MDA levels and MPO activity were increased. Furthermore, TNF-alpha, IL-1 beta, and amylase lipase levels were also significantly increased. On the other hand, lycopene pretreatment reserved all these biochemical indices as well as histopathologic alterations that were induced by cerulein. Conclusions. According to the results, lycopene protects the pancreatic tissues from oxidative damage induced by cerulein, and this effect possibly involves the inhibition of neutrophil infiltration and lipid peroxidation. These results suggest that high dietary intake of tomatoes may have protective effects against acute pancreatitis. (C) 2012 Elsevier Inc. All rights reserved.Publication Metadata only Aqueous garlic extract inhibits protamine sulfate-induced bladder damage(KARGER, 2006) ERCAN, FERİHA; Zeybek, A; Cikler, E; Saglam, B; Ercan, F; Cetinel, S; Sener, GThis morphological and biochemical study aims to investigate the antioxidant effects of chronic administration of aqueous garlic extract (AGE) on protamine sulfate (PS)-induced bladder injury. Wistar albino female rats were catheterized and intravesically infused with phosphate-buffered solution (control group) or PS (PS group) dissolved in phosphate-buffered solution. In the PS + AGE group after the PS instillation, AGE (1 ml/kg, i. p., corresponding to 250 mg/kg) was injected intraperitoneally for 3 days. Bladder morphology was investigated by light and scanning electron microscopy. Tissue samples were also obtained to determine bladder malondialdehyde (MDA) and glutathione levels. In the PS group, ulcerated areas, an irregular mucus layer, inflammatory cell infiltration and an increased number of mast cells were observed. In the PS + AGE group a relatively normal urothelial topography, glycosaminoglycan layer and a decreased number of mucosal mast cells and inflammatory cells were observed. Increased MDA levels as a result of PS induction led us to propose that free radicals may have a critical role in this injury. The significant decrease in MDA and increase in glutathione levels in the PS + AGE group was in accordance with morphological findings. Based on the results, AGE treatment significantly prevented PS-induced degenerative morphological and biochemical changes of urinary bladder mucosa. Copyright (c) 2006 S. Karger AG, Basel.