Person: ÇETİNEL, ŞULE
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ÇETİNEL
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ŞULE
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Publication Metadata only Mesna (2-mercaptoethane sulfonate) prevents ischemia/reperfusion induced renal oxidative damage in rats(PERGAMON-ELSEVIER SCIENCE LTD, 2004) ŞENER, GÖKSEL; Kabasakal, L; Sehirli, AO; Cetinel, S; Cikler, E; Gedik, N; Sener, GReoxygenation of the ischemic tissue promotes the generation of various reactive oxygen metabolites (ROM) which are known to have deleterious effects on various cellular functions. This study was designed to determine the possible protective effect of mesna (2-Mercaptoethane Sulfonate) 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 6 h of reperfusion. Mesna (MESNA, 150 mg/kg, i.p.; an effective dose against I/R injury) or vehicle was administered twice, 15 min prior to ischemia and immediately before the reperfusion period. At the end of the reperfusion period, rats were killed by decapitation. Kidney samples were taken for histological examination or determination of the free radicals, renal malondialdehyde (MDA) and glutathione (GSH) levels, and myeloperoxidase (MPO) activity. Renal tissue collagen content, as a fibrosis marker was also determined. Creatinine and urea concentrations in blood were measured for the evaluation of renal function. The results demonstrated that renal I/R caused nephrotoxicity, as evidenced by increases in blood urea and creatinine levels, which was reversed by MESNA treatment. Increased free radical levels, as assessed by nitroblue-tetrazolium test were reduced with MESNA. Moreover, the decrease in GSH and increases in MDA levels, and MPO activity induced by I/R indicated that renal injury involves free radical formation. Treatment of rats with MESNA restored the reduced GSH levels while it decreased MDA levels as well as MPO activity. Increased collagen contents of the kidney tissues by I/R were reversed back to the control levels by MESNA treatment. Since MESNA administration reversed these oxidant responses, improved renal function and microscopic damage, it seems likely that MESNA protects kidney tissue against I/R induced oxidative damage. (C) 2004 Elsevier Inc. All rights reserved.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 Metadata only Oxytocin alleviates oxidative renal injury in pyelonephritic rats via a neutrophil-dependent mechanism(ELSEVIER SCIENCE INC, 2006) VELİOĞLU ÖĞÜNÇ, AYLİZ; Biyikli, Nese Karaaslan; Tugtepe, Halil; Sener, Goksel; Velioglu-Ogunc, Ayliz; Cetinel, Sule; Midillioglu, Sukru; Gedik, Nursal; Yegen, Berrak C.Background: Urinary tract infection (UTI) may cause inflammation of the renal parenchyma and may lead to impairment in renal function and scar formation. Oxidant injury and reactive oxygen species (ROS) have been found responsible in the pathogenesis of UTI. The neurohypophyseal hormone oxytocin (OT) facilitates wound healing and is involved in the modulation of immune and inflammatory processes. We investigated the possible therapeutic effects of OT against Eschericia coli induced pyelonephritis in rats both in the acute and chronic setting. Methods: Twenty-four Wistar rats were injected 0.1 ml solution containing E. coli ATCC 25922 10(10) colony forming units/ml into left renal medullae. Six rats were designed as sham group and were given 0.1 ml 0.9% NaCl. Pyelonephritic rats were treated with either saline or OT immediately after surgery and at daily intervals. Half of the pyelonephritic rats were decapitated at the 24th hour of E. coli infection, and the rest were followed for 7 days. Renal function tests (urea, creatinine), systemic inflammation markers [lactate dehydrogenase (LDH) and tumor necrosis factor alpha (TNF-alpha)] and renal tissue malondialdehyde (MDA) as an end product of lipid peroxidation, glutathione (GSH) as an antioxidant parameter and myeloperoxidase (MPO) as an indirect index of neutrophil infiltration were studied. Results: Blood urea, creatinine, and TNF-a levels were increased, renal tissue MDA and MPO levels were elevated and GSH levels were decreased in both of the pyelonephritic (acute and chronic) rats. All of these parameters and elevation of LDH at the late phase were all reversed to normal levels by OT treatment. Conclusion: OT alleviates oxidant renal injury in pyelonephritic rats by its anti-oxidant actions and by preventing free radical damaging cascades that involves excessive infiltration of neutrophils. (c) 2006 Elsevier Inc. All rights reserved.Publication Metadata only The protective effect of oxytocin on renal ischemia/reperfusion injury in rats(ELSEVIER SCIENCE BV, 2007) YEGEN, BERRAK; Tugtepe, Halil; Sener, Goksel; Biyikli, Nese Karaaslan; Yuksel, Meral; Cetinel, Sule; Gedik, Nursal; Yegen, Berrak C.Aim: Oxytocin was previously shown to have anti-inflammatory effects in different inflammation models. The major objective of the present study was to evaluate the protective role of oxytocin (OT) in protecting the kidney against ischemia/reperfusion (I/R) injury. Materials and methods: Male Wistar albino rats (250-300 g) were unilaterally nephrectornized, and subjected to 45 min of renal pedicle occlusion followed by 6 It of reperfusion. OT (1 mg/kg, ip) or vehicle was administered 15 min prior to ischemia and was repeated immediately before the reperfusion period. At the end of the reperfusion period, rats were decapitated and kidney samples were taken for histological examination or determination of malondialdehyde (MDA), an end product of lipid peroxidation; glutathione (GSH), a key antioxidant; and myeloperoxidase (MPO) activity, an index of tissue neutrophil infiltration. Creatinine and urea concentrations in blood were measured for the evaluation of renal function, while TNF-alpha and lactate dehydrogenase (LDH) levels were determined to evaluate generalized tissue damage. Formation of reactive oxygen species in renal tissue samples was monitored by chemiluminescence technique using luminol and lucigenin probes. Results: The results revealed that I/R injury increased (p < 0.01-0.001) serum urea, creatinine, TNF-alpha and LDH levels, as well as MDA, MPO and reactive oxygen radical levels in the renal tissue, while decreasing renal GSH content. However, alterations in these biochemical and histopathological indices due to l/R injury were attenuated by OT treatment (P < 0.05-0.001). Conclusions: Since OT administration improved renal function and microscopic damage, along with the alleviation of oxidant tissue responses, it appears that oxytocin protects renal tissue against I/R-induced oxidative damage. (c) 2006 Elsevier B.V. All rights reserved.Publication Metadata only Oxidative renal damage in pyelonephritic rats is ameliorated by montelukast, a selective leukotriene CysLT1 receptor antagonist(ELSEVIER SCIENCE BV, 2007) VELİOĞLU ÖĞÜNÇ, AYLİZ; Tugtepe, Halil; Sener, Goksel; Cetinel, Sule; Velioglu-Ogunc, Ayliz; Yegen, Berrak C.Urinary tract infections may induce severe inflammation, transient impairment in renal function and scar formation, ranging in severity from acute symptomatic pyelonephritis to chronic pyelonephritis, which have a potential to lead to renal failure and death. The present study aimed to investigate the possible protective effect of montelukast, a selective antagonist of cysteinyl leukotriene receptor I (leukotriene CysLT1), against Escherichia coli-induced oxidative injury and scarring in renal tissue. Wistar rats were injected 0.1 ml of E. coli (ATCC 25922 10(10) cfu/ml) or saline into left renal medullae. Six rats were assigned as the sham group and were given 0.1 ml 0.9% NaCl. Pyelonephritic rats were treated with either saline or montelukast immediately after surgery and at daily intervals. Twenty-four hours or one week after E. coli injection, rats were decapitated and the kidney samples were taken for histological examination or determination of renal malondialdehyde, glutathione (GSH) levels, myeloperoxidase (MPO) activity, and collagen contents. Formation of reactive oxygen species in renal tissue samples was monitored by using chemiluminescence technique with luminol and lucigenin probes. Creatinine, blood urea nitrogen and lactate dehydrogenase (LDH) activity were measured in the serum samples. E. coli inoculation caused significant increases in malondialdehyde level, MPO activity, chemiluminescence levels and collagen content, while GSH level was decreased in the renal tissues (p < 0.05-0.001). On the other hand, serum TNF-alpha, LDH, blood urea nitrogen and serum creatinine levels were elevated in the pyelonephritic rats as compared to control group. Leukotriene CysLT1 receptor antagonist montelukast reversed all these biochemical indices, as well as histopathological alterations, that were induced by acute pyelonephritis. It seems likely that montelukast protects kidney tissue by inhibiting neutrophil infiltration, balancing oxidant-antioxidant status, and regulating the generation of inflammatory mediators suggesting a future role for leukotriene CysLT1 receptor antagonists in the treatment of pyclonephritis. (c) 2006 Elsevier B.V. All rights reserved.Publication Open Access Ginkgo biloba extract reduces naphthalene-induced oxidative damage in mice(JOHN WILEY & SONS LTD, 2007-01) BECEREN, AYFER; Tozan, Ayfer; Sehirli, Ozer; Omurtag, Gulden Z.; Cetinel, Sule; Gedik, Nursal; Sener, GokselThis investigation elucidated the role of free radicals in naphthalene-induced toxicity and protection by Ginkgo biloba extract (EGb). BALB-c mice of either sex were administered with naphthalene (100 mg/kg; i.p.) for 30 days, along with either saline or EGb (150 mg/kg, orally). At the end of the experiment, following decapitation, lung, liver and kidney tissue samples were taken for histological examination or determination of malondialdehyde (MDA), glutathione (GSH), myeloperoxidase (MPO) activity and collagen contents. In addition, proinflammatory cytokines (TNF-alpha and IL-beta) and total antioxidant capacity (AOC) were assayed in the plasma, while lactate dehydrogenase (LDH) activity was assayed in serum samples. The results revealed that naphthalene caused a significant decrease in GSH level, and significant increases in MDA level, MPO activity and collagen content of tissues. Similarly, plasma cytokines, as well as serum LDH activity, were elevated while AOC was decreased in the naphthalene group compared with the control group. On the other hand, EGb treatment reversed all these biochemical indices. The results demonstrate that EGb extract, by balancing the oxidant-antioxidant status and inhibiting the generation of proinflammatory cytokines and neutrophil infiltration, protects against naphthalene-induced oxidative organ injury. Copyright (c) 2006 John Wiley & Sons, Ltd.Publication Metadata only Taurine ameliorates water avoidance stress-induced degenerations of gastrointestinal tract and liver(SPRINGER, 2006) ERCAN, FERİHA; Zeybek, Ali; Ercan, Feriha; Cetinel, Sule; Cikler, Esra; Saglam, Beyhan; Sener, GokselWe investigated the role of taurine, is a potent free radical scavenger, on water avoidance stress (WAS)induced degeneration of the gastric, ileal, and colonic mucosa and liver parenchyma. Wistar albino rats were exposed to chronic WAS (WAS group) 2 hr daily for 5 days. After exposing animals to chronic WAS (WAS + taurine group), 50 mg/kg taurine was injected IP for 3 days. Control animals received vehicle solution only. The stomach, ileum, colon, and liver samples were investigated under light microscope for histopathologic changes. To demonstrate the topography of the luminal mucosa of the stomach, ileum, and colon, scanning electron microscope was used and for hepatocyte ultastructure transmission electron microscope was used. Malondialdehyde (MDA, a biomarker of oxidative damage) and glutathione (GSH, a biomarker of protective oxidative injury) levels were also determined in all tissues. In the WAS group, the stomach epithelium showed ulceration in some areas, dilatations of the gastric glands, and degeneration of gastric glandular cells; prominent congestion of the capillaries was apparent. In the WAS group, severe vascular congestion was observed along with degeneration of ileal and colonic epithelium. Prominent vascular congestion and dilated sinusoids, activated Kupffer cells, dilated granular endoplasmic reticulum membranes, and focal pyknotic nuclei were observed in liver parenchyma. MDA levels (stomach, P < 0.01; ileum, colon, and liver P < 0.05) were increased and GSH levels (P < 0.01) were decreased in all tissues in the WAS group compared with the control group. The morphology of gastric, ileal, and colonic mucosa and liver parenchyma in the WAS + taurine group (stomach and ileum, P < 0.05; colon and liver, P < 0.01) showed a significant amelioration when compared to the WAS g roup. Increased MDA and decreased GSH levels in the WAS group were ameliorated with taurine treatment. Based on the results, taurine supplementation effectively attenuates the oxidative damage of gastrointestinal mucosa and liver because of WAS induction possibly by its antioxidant effects.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.