Person: ÇETİNEL, ŞULE
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ÇETİNEL
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ŞULE
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Publication Metadata only Acetaminophen-induced toxicity is prevented by beta-D-glucan treatment in mice(ELSEVIER SCIENCE BV, 2006) VELİOĞLU ÖĞÜNÇ, AYLİZ; Toklu, Hale Z.; Sehirli, A. Ozer; Velioglu-Ogunc, Ayliz; Cetinel, Sule; Sener, GokselThe protective effect of beta-glucan against oxidative injury caused by acetaminophen was studied in mice liver. BALB-c mice (25-30 g) were pretreated with beta-D-glucan (50 mg/kg, p.o.) for 10 days and on the 11th day they received an overdose of acetaminophen (900 mg/kg, i.p.). Four hours after the acetaminophen injection, mice were decapitated and their blood was taken to determine serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH) and tumor necrosis factor-alpha (TNF-alpha) levels. Tissue samples of the liver were taken for histological examination or for the determination of levels of malondialdehyde, an end product of lipid peroxidation; glutathione (GSH), a key antioxidant; and myeloperoxidase activity, an index of tissue neutrophil infiltration. The formation of reactive oxygen species in hepatic tissue samples was monitored by using the chemilummescence technique with luminol and lucigenin probes. Acetaminophen caused a significant decrease in the GSH level of the tissue, which was accompanied with significant increases in the hepatic luminol and lucigenin chemiluminescence values, malondialdehyde level, MPO activity and collagen content. Similarly, serum ALT, AST levels, as well as LDH and TNF-alpha, were elevated in the acetaminophen-treated group when compared with the control group. On the other hand, P-D-glucan treatment reversed all these biochemical indices, as well as histopathological alterations that were induced by acetaminophen. In conclusion, these results suggest that beta-D-glucan exerts cytoprotective effects against oxidative injury through its antioxidant properties and may be of therapeutic use in preventing acetaminophen toxicity. (c) 2006 Elsevier B.V. All rights reserved.Publication Metadata only Protective effects of resveratrol against acetaminophen-induced toxicity in mice(WILEY, 2006) VELİOĞLU ÖĞÜNÇ, AYLİZ; Sener, Goksel; Toklu, Hale Z.; Sehirli, A. Ozer; Velioglu-Ogunc, Ayliz; Cetinel, Sule; Gedik, NursalThis investigation elucidates the role of free radicals in acetaminophen (AA)-induced toxicity and the possible protection by resveratrol (RVT). BALB-c mice were injected with a single dose of 900 mg/kg AA to induce toxicity, while RVT administred in a dose of 30 mg/kg i.p. following AA. Mice were sacrificed 4 h after AA injection to determine 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. Formation of reactive oxygen species in hepatic tissue samples was monitored by using chemiluminescence (CL) technique with luminol and lucigenin probe. ALT, AST levels and TNF-alpha were increased significantly after AA treatment, and reduced with RVT. AA caused a significant decrease in GSH levels while MDA levels and MPO activity were increased in liver tissues. On the other hand when RVT administered following AA, depletion of GSH and accumulation of MDA and neutrophil infiltration were reversed back to control. Furthermore increased luminol and lucigenin CL levels in the AA group reduced by RVT treatment. Our results implicate that AA causes oxidative damage in hepatic tissues and RVT, by its potent antioxidant effects protects the liver tissue. These data suggest that RVT may be of therapeutic use in preventing hepatic oxidative injury due to AA toxicity. (c) 2006 Elsevier Ireland Ltd. All rights reserved.Publication Open Access Investigation of the Effects of Edaravone on Valproic Acid Induced Tissue Damage in Pancreas(MARMARA UNIV, FAC PHARMACY, 2017-06-20) YARAT, AYŞEN; Oktay, Sehkar; Alev-Tuzuner, Burcin; Tunali, Sevim; Ak, Esin; Emekli-Alturfan, Ebru; Tunali-Akbay, Tugba; Koc-Ozturk, Leyla; Cetinel, Sule; Yanardag, Refiye; Yarat, AysenValproic acid (VPA), an effective antiepileptic and anticonvulsant drug, has some toxic side effects due to causing elevated oxidant production. The aim of this study is to investigate the effects of edaravone, a potent free radical scavenger on VPA induced toxicity and tissue damage by biochemical and histological examinations on pancreas. Female Sprague Dawley rats were divided into four groups as follows; control, edaravone, VPA, VPA+edaravon. VPA and edaravone were injected intraperitonally for seven days. Total protein, lipid peroxidation (LPO), sialic acid (SA) and glutathione (GSH) levels and alkaline phosphatase (ALP), tissue factor (TF), superoxide dismutase (SOD), glutathione-S-transferase GST), catalase (CAT), glutathione peroxidase (GPx) and myeloperoxidase (MPO) activities were determined in pancreas homogenates. In VPA given group, LPO and SA levels, and ALP, TF, MPO activities significantly increased and GST, CAT, GPx activities significantly decreased compared to control group. A marked morphological damage was detected in the VPA group. Ameliorative effects of edaravone were observed in SA, TF, CAT, GPx parameters and histological examination in the VPA group. Therefore, edaravone may be effective in moderation and/or reduction of toxic effects of VPA on pancreas.Publication Metadata only alpha-lipoic acid protects against renal ischaemia-reperfusion injury in rats(BLACKWELL PUBLISHING, 2008) YÜKSEL, MERAL; Sehirli, Oezer; Sener, Emre; Cetinel, Ule; Yueksel, Meral; Gedik, Nursal; Sener, Goeksel1. Oxygen free radicals are important components involved in the pathophysiological processes observed during ischaemia-reperfusion (I/R). The present study was designed to assess the possible protective effect of et-lipoic acid (ALA) on renal I/R injury. 2. Wistar albino rats were unilaterally nephrectomized and subjected to 45 min renal pedicle occlusion followed by 24 h reperfusion. Saline or ALA (100 mg/kg, i.p.) was administered 15 min prior to ischaemia and immediately before the reperfusion period. At the end of 24 h, rats were decapitated and trunk blood was collected. Creatinine, blood urea nitrogen (BUN) and lactate dehydrogenase (LDH) activity were measured in serum samples, whereas tumour necrosis factor (TNF)-alpha, interleukin (IL)-1 beta, IL-6, 8-hydroxydeoxyguanosine (8-OHdG) and total anti-oxidant capacity (AOC) were assayed in plasma samples. 3. Kidney samples were taken for the determination of tissue malondialdehyde (MDA) and glutathione (GSH) levels, as well as Na/K-ATPase and myeloperoxidase (MPO) activity. The formation of reactive oxygen species in renal tissue samples was monitored using a chemiluminescence (CL) technique with luminol and lucigenin probes. Oxidant-induced tissue fibrosis was determined by tissue collagen content and the extent of tissue injury was analysed microscopically. 4. Ischaemia-reperfusion caused a significant increases in blood creatinine, BUN, LDH, IL-1 beta, IL-6, TNF-alpha and 8-OHdG, whereas AOC was decreased. In kidney samples from the I/R group, MDA, MPO, collagen and CL levels were found to be increased significantly; however, glutathione levels and Na/KATPase activity were decreased. Conversely, ALA treatment reversed all these biochemical indices, as well as histopathological alterations induced by I/R. 5. In conclusion, these data suggest that ALA reverses I/R-induced oxidant responses and improves microscopic damage and renal function. Thus, it seems likely that ALA protects kidney tissues by inhibiting neutrophil infiltration, balancing the oxidant-anti-oxidant status and regulating the generation of inflammatory mediators.Publication Metadata only Changes in caveolin-1 expression and vasoreactivity in the aorta and corpus cavernosum of fructose and streptozotocin-induced diabetic rats(ELSEVIER, 2010) ELÇİOĞLU, HATİCE KÜBRA; Elcioglu, Kuebra H.; Kabasakal, Levent; Cetinel, Sule; Conturk, Gazi; Sezen, Sena F.; Ayanoglu-Dulger, GuelHyperglycemia is a common defining feature in the development of endothelial dysfunction which plays a key role in the pathogenesis of both type 1 and type 2 diabetes. Caveolin-1 is the main structural component of caveolae which might be involved in the pathophysiology of macrovascular complications of diabetes. In this study we aimed to observe the effect of caveolin-1 on functional responses of aorta and corpus cavernosum in the streptozotocin and fructose-induced diabetes groups. Type 1 diabetes was induced by intraperitoneal administration of streptozotocin (60 mg/kg),. Type 2 diabetes by adding fructose in the rat's drinking water (10% (w/v)) for 8 weeks. For insulin treatment; rats were treated with insulin (6 U/kg) for 8 weeks. In Type I and Type II diabetic groups the contractile responses of corpus cavernosum strips to phenylephrine (EC50:1.82 x 10(-5) M;1.47 x 10(-5) M, respectively)and relaxation responses to acetylcholine (EC50:7.5 x 10(-5) M;4.48 x 10(-5) M, respectively)were significantly impaired. Contractile responses of aortic-strips to phenylephrine in diabetic groups were markedly decreased (EC50:3.7. 10(-7) M;2.61. 10(-7) M respectively) and dose-dependent relaxation responses to acetylcholine were also attenuated (EC50:3.23 . 10(-6)M; 2.0. 10(-6)M respectively). Treatment with insulin improved the functional responses in the aorta and corpus cavernosum. Protein expression of caveolin-1 was increased in the aorta and corpus cavernosum of the diabetic groups, but this increase seen in the streptozotocin group was more significant than the fructose group. Our findings indicate that an attenuation of the functional responses in both diabetes groups were probably associated with an enhanced expression of caveolin-1, and therefore a decrease in the eNOS activity with a concomitant decrease in NO synthesis. (C) 2010 Elsevier B.V. All rights reserved.Publication Metadata only The Effects of Melatonin on Ethylene Glycol-induced Nephrolithiasis: Role on Osteopontin mRNA Gene Expression(ELSEVIER SCIENCE INC, 2017) ŞENER, GÖKSEL; Sener, Tarik Emre; Sener, Goksel; Cevik, Ozge; Eker, Pinar; Cetinel, Sule; Traxer, Olivier; Tanidir, Yiloren; Akbal, CemOBJECTIVE To evaluate the protective effects of melatonin (Mel) on an ethylene glycol (EG)-induced nephrolithiasis model in rats. MATERIALS AND METHODS Thirty-two Wistar albino rats were divided into 4 groups: control, EG, prevention Mel (Mel + EG + Mel), and therapeutic Mel (EG + Mel). EG (0.75%) was added to drinking water to create nephrolithiasis model. The EG group received EG and the Mel + EG + Mel group received both EG and Mel for 8 weeks. In the EG + Mel group, EG is given for 8 weeks and Mel is given for the last 4 weeks of the experiment. At the end of experimental period, urine, blood samples, and tissues were collected. RESULTS In 24-hour urine samples, calcium, citrate, and creatinine levels were decreased and oxalate levels were increased in the EG group, whereas Mel prevention and Mel treatment reversed these parameters back to control levels. Malondialdehyde, glutathione activities, myeloperoxidase, superoxide dismutase levels, and caspase-3 activity showed improvements in the Mel-treated groups when compared with the EG group. 8-Hydroxydeoxyguanosine, matrix metalloproteinase 9 levels, N-acetyl-beta-glucosaminidase activity, and osteopontin mRNA expression were elevated in the EG group and decreased back to control levels in the Mel + EG + Mel and EG + Mel groups. Histological examination showed improvement in the Mel-treated groups when compared with the EG group. CONCLUSION Mel can prevent crystalluria and kidney damage due to crystal formation and aggregation. It can be considered as a potential prophylactic and protective agent in high-risk patients with urinary stone formation or recurrence if supported by further clinical studies. (C) 2016 Elsevier Inc.Publication Metadata only Ginkgo biloba extract ameliorates ischemia reperfusion-induced renal injury in rats(ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD, 2005) VELİOĞLU ÖĞÜNÇ, AYLİZ; Sener, G; Sener, E; Sehirli, O; Ogunc, AV; Cetinel, S; Gedik, N; Sakarcan, AThere is increasing evidence to suggest that reactive oxygen metabolites (ROMs) play a role in the pathogenesis of ischemia/reperfusion injury (I/R) in the kidney. This study was designed to determine the possible protective effect of Ginkgo biloba extract (EGb) on renal ischemia/reperfusion (I/R) injury. Wistar albino rats were unilaterally nephrectomized, and 15 days later they were subjected to 45 min of renal pedicle occlusion followed by 6h of reperfusion. Ginkgo biloba extract (EGb) (50mg kg(-1) day(-1)) or saline was administered twice, 15 min prior to ischemia and immediately before the reperfusion period. At the end of the treatment period, all rats were decapitated. Kidney samples were taken for histological examination or detennination of the renal malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity and collagen content. Production of reactive oxidants was monitored by chemiluminescence (CL) assay. Creatinine and urea concentrations in blood were measured for the evaluation of renal function. Tumor necrosis factor-alpha (TNF-alpha) and lactate dehydrogenase (LDH) were also assayed in serum samples. Ischemia/reperfusion caused a significant decrease in GSH level, which was accompanied with significant increases in MDA level, MPO activity and collagen content of kidney tissues. Similarly, serum BUN and creatinine levels, as well as LDH and TNF-alpha, were elevated in the I/R group as compared to control group. On the other hand, EGb treatment reversed all these biochemical indices, as well as histopathological alterations, which were induced by I/R. The findings imply that ROMs play a causal role in I/R-induced renal injury and EGb exerts renoprotective effects probably by the radical scavenging and antioxidant activities. (c) 2005 Elsevier Ltd. All rights reserved.Publication Metadata only Protective and therapeutic effects of resveratrol on acetic acid-induced gastric ulcer(TAYLOR & FRANCIS LTD, 2009) YEGEN, BERRAK; Solmaz, Ali; Sener, Goeksel; Cetinel, Sule; Yueksel, Meral; Yegen, Cumhur; Yegen, Berrak C.Sprague Dawley rats of both sexes were injected with either saline or RVT (10 mg/kg) either before or after acetic acid ulcer induction and decapitated 3, 5 or 10 days after ulcer. In the saline-treated ulcer groups, macroscopically evident ulcers were observed, while RVT-pretreated or RVT-treated groups had lower macroscopic ulcer scores. Likewise, the microscopic damage scores were lower for the RVT-administered groups. Gastric myeloperoxidase activity, malondialdehyde, collagen and tumour necrosis factor-alpha levels, as well as luminol- and lucigenin-enhanced chemiluminescence levels that were elevated in the saline-administered ulcer groups, were depressed with both RVT-pretreatment and RVT-treatment. Moreover, depleted glutathione levels in the ulcer groups were increased back to control levels by both pre- and post-treatments of RVT. Results demonstrate that resveratrol has both protective and therapeutic effects on oxidative gastric damage by suppressing pro-inflammatory cascades, including the activation of pro-inflammatory cytokines, accumulation of neutrophils and release of oxygen-derived free radicals.Publication Open Access Protective effect of betaine against burn-induced pulmonary injury in rats(TURKISH ASSOC TRAUMA EMERGENCY SURGERY, 2015) YEGEN, BERRAK; Sehirli, Ahmet Ozer; Satilmis, Burcu; Tetik, Sermin; Cetinel, Sule; Yegen, Berrak; Aykac, Asli; Sener, GokseiBACKGROUND: This study was designed to determine possible protective effect of betaine treatment against oxidative injury in pulmonary tissue induced with thermal trauma. METHODS: Under ether anesthesia, shaved dorsum of Wistar albino rats was exposed to a 90 degrees C water bath for 10 seconds to induce burn injury. Betaine was administered orally (250 mg/kg) for a period of 21 days before burn injury, and single dose of betaine was administered after thermal injury. Control group rats were exposed to 25 degrees C water bath for 10 seconds. Upon conclusion of experiment, rats were decapitated and blood was collected for analysis of pro-inflammatory cytokines and lactate dehydrogenase (LDH) activity. Lung tissue samples were taken to determine malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO), and Na+/K+-ATPase activity, in addition to histological analysis. RESULTS: Burn injury caused significant increase in both cytokine levels and LDH activity. In lung samples, raised MDA levels, MPO activity, and reduced GSH levels and Na+/K+-ATPase activity were found due to burn injury. CONCLUSION: Treatment of rats with betaine significantly restored GSH level and Na+/K+-ATPase activity, and decreased MDA level and MPO activity. According to the findings of the present study, betaine significantly diminishes burn-induced damage in tissue.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.