Person: YEGEN, BERRAK
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YEGEN
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BERRAK
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Publication Metadata only Melatonin protects against oxidative organ injury in a rat model of sepsis(SPRINGER, 2005) YEGEN, BERRAK; Sener, G; Toklu, H; Kapucu, C; Ercan, F; Erkanli, G; Kacmaz, A; Tilki, M; Yegen, BCPurpose. Based on the potent antioxidant effects of melatonin, we investigated the putative protective role of melatonin against sepsis-induced oxidative organ damage in rats. Methods. Sepsis was induced by cecal ligation and puncture (CLP) in Wistar albino rats. Animals subjected to CLP and sham-operated control rats were given saline or melatonin 10 mg/kg intraperitoneally 30 min before and 6 h after the operation. The rats were killed 16 h after the operation and the biochemical changes were investigated in the liver, kidney, heart, lung, diaphragm, and brain tissues by examining malondialdehyde (MDA) and glutathione (GSH) levels, and myeloperoxidase (MPO) activity. We also examined the tissues microscopically. Results. Sepsis resulted in a significant decrease in GSH levels and a significant increase in MDA levels and MPO activity (P < 0.05-P < 0.001) showing oxidative damage, which was confirmed by histological examination. Melatonin clearly reversed these oxidant responses and the microscopic damage, demonstrating its protective effects against sepsis-induced oxidative organ injury. Conclusion. The increase in MDA levels and MPO activity and the concomitant decrease in GSH levels demonstrate the role of oxidative mechanisms in sepsis-induced tissue damage. Melatonin, by its free radical scavenging and antioxidant properties, ameliorated oxidative organ injury. Thus, supplementing antiseptic shock treatment with melatonin may be beneficial in the clinical setting.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 Resveratrol protects against irradiation-induced hepatic and ileal damage via its anti-oxidative activity(TAYLOR & FRANCIS LTD, 2009) VELİOĞLU ÖĞÜNÇ, AYLİZ; Velioglu-Ogunc, Ayliz; Sehirli, Ozer; Toklu, Hale Z.; Ozyurt, Hazan; Mayadagli, Alpaslan; Eksioglu-Demiralp, Emel; Erzik, Can; Cetinel, Sule; Yegen, Berrak C.; Sener, GoekselThe present study was undertaken to determine whether resveratrol (RVT) could ameliorate ionizing radiation-induced oxidative injury. After a 10-days pre-treatment with RVT (10 mg/kg/day p.o.), rats were exposed to whole-body IR (800 cGy) and the RVT treatment was continued for 10 more days after the irradiation. Irradiation caused a significant decrease in glutathione level, while malondialdehyde levels, myeloperoxidase activity and collagen content were increased in the liver and ileum tissues. Similarly, plasma lactate dehydrogenase and pro-inflammatory cytokine levels, 8-hydroxy-2'-deoxyguanosine and leukocyte apoptosis were elevated, while antioxidant-capacity was reduced in the irradiated rats as compared with the control group. Furthermore, Na-1, K-1 -ATPase activity was inhibited and DNA fragmentation was increased in the ileal tissues. Resveratrol treatment reversed all these biochemical indices, as well as histopathological alterations induced by irradiation. In conclusion, supplementing cancer patients with adjuvant therapy of resveratrol may have some benefit for a more successful radiotherapy.Publication Metadata only Estrogen Protects against Oxidative Multiorgan Damage in Rats with Chronic Renal Failure(TAYLOR & FRANCIS LTD, 2009) YEGEN, BERRAK; Kasimay, Oezguer; Sener, Goeksel; Cakir, Baris; Yueksel, Meral; Cetinel, Sule; Contuk, Gazi; Yegen, Berrak C.The impact of sex dimorphism on chronic renal failure (CRF)-induced oxidative multiorgan damage and the effects of estradiol (E-2) loss and E-2 supplementation on the progress of CRF were studied. Sprague-Dawley rats underwent 5/6 nephrectomy (CRF), and a group of female rats had bilateral ovariectomy (OVX), while the sham-operated rats had no nephrectomy or OVX. Rats received either estradiol propionate (50 mu g/kg/day) or vehicle for six weeks. Serum BUN levels were elevated in both male and female CRF groups treated with vehicle, while creatinine level was not significantly changed in the female CRF group. CRF-induced elevation in serum TNF-alpha of male rats was abolished when the animals were treated with E-2, while OVX exaggerated TNF-alpha response. In OVX and male rats with CRF, E-2 treatment reversed the malondialdehyde elevations in all the studied tissues (kidney, heart, lung, ileum, brain, liver, and gastrocnemius muscle), while depletion of glutathione in these tissues was prevented by E-2 treatment. Similarly, increased levels of myeloperoxidase activity, lucigenin chemiluminescence, and collagen in most of the tissues were reversed by E-2 treatment. The findings show that the extent of tissue injuries was relatively less in females, while ovariectomy exacerbated all the indices of oxidative injury. Moreover, the administration of E-2, with its potent anti-oxidant and anti-inflammatory effects, markedly improved CRF-induced systemic inflammatory outcomes in both male and female rats by depressing tissue neutrophil infiltration and modulating the release of inflammatory cytokines.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 Ghrelin alleviates biliary obstruction-induced chronic hepatic injury in rats(ELSEVIER, 2008) YEGEN, BERRAK; Iseri, Sevgln Oezlem; Sener, Goeksel; Saglam, Beyhan; Ercan, Feriha; Gedik, Nursal; Yegen, Berrak C.Background: Reactive oxygen species and oxidative stress are implicated in hepatic stellate cell activation and liver fibrosis, which are initiated by recruitment of inflammatory cells and by activation of cytokines. Objective: The possible anti-oxidant and anti-inflammatory effects of ghrelin were evaluated in a hepatic fibrosis model in rats with bile duct ligation (BDL). Methods: Under anesthesia, bile ducts of Sprague Dawley rats were ligated, and half of the rats were subcutaneously administered with ghrelin (10 ng/kg/day) and the rest with saline for 28 days. Sham-operated control groups were administered saline or ghrelin. On the 28th day of the study, rats were decapitated and malondialdehyde (NIDA) content - an index of lipid peroxidation, and myeloperoxidase (MPO) activity - an index of neutrophil infiltration - were determined in the liver tissues. Oxidant-induced tissue fibrosis was determined by collagen contents, while the hepatic injury was analyzed microscopically. Serum aspartate aminotransferase (AST), alanine aminotransferase (ALT) levels and lactate dehydrogenase (LDH) levels were determined to assess liver function and tissue damage, respectively. Pro-inflammatory cytokines; TNF-alpha, IL-1 beta and IL-6 were also assayed in plasma samples. Results: In the saline-treated BDL group, hepatic NIDA levels, MPO activity and collagen content were increased (p < 0.001), suggesting oxidative organ damage, as confirmed histologically. In the ghrelin-treated BDL group, however, all of the oxidant responses were reversed significantly (p < 0.05-p < 0.001). Serum AST, ALT, LDH levels, and cytokines were elevated in the BDL group as compared to the control group, while this increase was significantly decreased by ghrelin treatment. Conclusion: Owing to the anti-inflammatory and anti-oxidant effect as demonstrated in our study, it is possible to speculate that exogenously administered ghrelin may possess an antifibrotic effect against biliary obstruction-induced liver fibrosis. Thus, it seems likely that ghrelin may be of potential therapeutic value in protecting the liver fibrosis and oxidative injury due to biliary obstruction. (c) 2007 Elsevier B.V. All rights reserved.Publication Metadata only Ghrelin improves burn-induced multiple organ injury by depressing neutrophil infiltration and the release of pro-inflammatory cytokines(ELSEVIER SCIENCE INC, 2008) YEGEN, BERRAK; Sehirli, Oezer; Sener, Emre; Sener, Goeksel; Cetinel, Sule; Erzik, Can; Yegen, Berrak C.Mechanisms of burn-induced skin and remote organ injury involve oxidant generation and the release of pro-inflammatory cytokines. In this study the possible antioxidant and anti-inflammatory effects of ghrelin were evaluated in a rat model of thermal trauma. Wistar albino rats were exposed to 90 degrees C bath for 10 s to induce thermal trauma. Ghrelin, was administered subcutaneously (10 ng/kg/day) after the burn injury and repeated twice daily. Rats were decapitated at 6 h and 48 h after burn injury and blood was collected for the analysis of pro-inflammatory cytokines (TNF-alpha and IL-1 beta), lactate dehydrogenase (LDH) activity and antioxidant capacity (AOC). In skin, lung and stomach tissue samples malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) and Na+-K+-ATPase activity were measured in addition to the histological analysis. DNA fragmentation ratio in the gastric mucosa was also evaluated. Burn injury caused significant increase in both cytokine levels, and LDH activity, while plasma ACC was found to be depleted after thermal trauma. On the other hand, in tissue samples the raised MDA levels, MPO activity and reduced GSH levels, Na+-K+-ATPase activity due to burn injury were found at control levels in ghrelin-treated groups, while DNA fragmentation in the gastric tissue was also reduced. According to the findings of the present study, ghrelin possesses a neutrophil-dependent anti-inflammatory effect that prevents burn-induced damage in skin and remote organs and protects against oxidative organ damage. (C) 2008 Elsevier Inc. All rights reserved.Publication Metadata only Ghrelin ameliorates pancreaticobiliary inflammation and associated remote organ injury in rats(WILEY, 2006) YEGEN, BERRAK; Kasimay, Ozgur; Iseri, Sevgin Ozlem; Barlas, Afsar; Bangir, Dilek; Yegen, Cumhur; Arbak, Serap; Yegen, Berrak C.The present study was designed to evaluate whether ghrelin could reduce organ injury and systemic inflammation induced by pancreaticobiliary obstruction. In Sprague-Dawley rats, either the bile duct (BDL) or common pancreaticobiliary duct (PBDL) was ligated or a sham operation was applied. BDL or PBDL rats received either ghrelin (10 ng/kg) or saline intraperitoneally immediately before the surgery and once a day until the rats were decapitated at 72 h. The pancreas, liver, lung and kidney were removed for the histological analysis, and for the determination of malondialdehyde (MDA), glutathione (GSH) levels and myeloperoxidase activity (MPO). MDA and MPO levels in all the tissues, which were elevated in PBDL group (p < 0.05-0.001), were reversed back to control levels in ghrelin-treated rats. In BDL group, elevations in hepatic MDA and MPO levels (p < 0.001) were also abolished by ghrelin treatment. In contrast to saline-treated group with severe pancreatic damage, ghrelin-treated rats demonstrated a moderate pancreatic and hepatic destruction accompanied with reduced pulmonary and renal damages. The results illustrate that ghrelin protects the hepatic and pancreatic tissues, as well as remote organs against oxidative injury, by a neutrophil-dependent mechanism. (c) 2006 Elsevier Ireland Ltd. All rights reserved.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 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.