Person: YEGEN, BERRAK
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YEGEN
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BERRAK
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Publication Metadata only Oxytocin ameliorates skin damage and oxidant gastric injury in rats with thermal trauma(ELSEVIER SCI LTD, 2008) YEGEN, BERRAK; Iseri, Sevgin Oezlem; Gedik, Ismail Ertugrul; Erzik, Can; Uslu, Bahar; Arbak, Serap; Gedik, Nursal; Yegen, Berrak C.Transient splanchnic vasoconstriction following major burns causes oxidative and/or nitrosative damage in gastrointestinal tissues due to ischemia, which is followed by reperfusion injury. Oxytocin (OT), a hypothalamic nonapeptide, possesses antisecretory and antiulcer effects, facilitates wound healing and is involved in immune and inflammatory processes. To assess the possible protective effect of oxytocin (OT) against burn-induced gastric injury, Sprague-Dawley rats (250-300 g) were randomly divided into three groups as control (n = 8), OT-treated burn (n = 8) and saline-treated burn (n = 8) groups. Under anesthesia, the shaved dorsal skin of rats was exposed to 90 degrees C water for 10 s to induce burn injury covering 30% of total body surface area in a standardized manner. Either oxytocin (5 mu g/kg) or saline was administered subcutaneously immediately after and at 24 h following burn, and the rats were decapitated at 48 h. Serum samples were assayed for TNF-alpha, and stomach was taken for the determination of malondialdehyde (MDA), myeloperoxidase (MPO) activity, DNA fragmentation rate (%) and histopathological examination. MDA and MPO were assayed for products of lipid peroxidation and as an index of tissue neutrophil infiltration, respectively. When compared to control group, burn caused significant increases in gastric MDA and MPO activity and increased microscopic damage scores at 48 h (p < 0.001). Oxytocin treatment reversed the burn-induced elevations in MDA and MPO levels and reduced the gastric damage scores (p < 0.001, p < 0.01), while TNF-alpha levels, which were increased significantly at 48th h after injury (p < 0.001), were abolished with OT treatment (p < 0.001). The results of this study suggest that oxytocin may provide a therapeutic benefit in diminishing burn-induced gastric inflammation by depressing tissue neutrophil infiltration and decreasing the release of inflammatory cytokines, but requires further investigation as a potential therapeutic agent in ameliorating the systemic effects of severe burn. (C) 2007 Elsevier Ltd and ISBI. All rights reserved.Publication Open Access Ghrelin Treatment Improves Lipid Metabolism and Hepatic Degeneration in Ovariectomized Rats(GAZI UNIV, FAC MED, 2020-01-01) YEGEN, BERRAK; Gurler, Esra Bihter; Ozbeyli, Dilek; Kaya, Ozlem Tugce Cilingir; Ercan, Feriha; Yegen, Berrak C.Objective: Metabolic disorders occurring in post-menopausal period increase the risk for development of fatty liver disease in women. Aim of the study was to evaluate possible effects of ghrelin on metabolic biomarkers and hepatic morphology in ovariectomized (OVT) rats. Methods:Under ketamine-chlorpromazine anesthesia (100 mg/kg, 0.75 mg/kg), Sprague-Dawley rats (n=12) underwent bilateral OVT, while control group had sham-surgery (n=6). Four weeks after surgery, half of OVT rats were treated intraperitonally with ghrelin (1 mg/kg/hafta) for 4 weeks, while others were not treated. Rats were euthanized by cardiac puncture at the end of 8th weeks, and serum levels of glucose, insulin, aspartate aminotransferase (AST), high-density lipoprotein (HDL), low-density lipoprotein (LDL), very low-density lipoprotein (VLDL), triglycerides, estradiol and progesterone were measured by an automated analyzer. Results: Increased body weights in OVT rats (p<0.001) recorded at the end of 2 months was not changed with ghrelin. Serum estradiol and progesterone levels were reduced (p<0.05) verifying altered gonadal hormone status, but insulin and glucose levels were not changed. Reduced HDL and increased LDL levels (p<0.0.5) were evident in non-treated OVX rats, while ghrelin treatment depressed LDL levels (p<0.0.5), but did not change HDL levels. However, ghrelin in OVT rats depressed triglycerides, VLDL and AST levels significantly (p<0.05). Moderate sinusoidal congestion, activated Kupffer cells and hepatocytes with ballooning degeneration was observed in non-treated OVT rats, while significant improvements were present in livers of ghrelin-treated rats. Conclusion: In conclusion, mild dyslipidemia and hepatic degeneration in early post-menopausal period appear to be attenuated by ghrelin treatment, and require further investigation.Publication Metadata only Burn-induced oxidative injury of the gut is ameliorated by the leukotriene receptor blocker montelukast(ELSEVIER SCI LTD, 2005) YEGEN, BERRAK; Kabasakal, L; Sener, G; Cetinel, S; Contuk, G; Gedik, N; Yegen, BCThere is increasing evidence that oxidative stress has an important role in the development of multiorgan failure after major burn injury. In the present study, we investigated whether the leukotriene receptor blocker montelukast is protective against burn-induced injury of the gut. Under brief ether anaesthesia, shaved dorsum of the rats was exposed to 90 degrees C (burn group) or 25 degrees C (control group) water bath for 10s. Montelukast (10mg/kg) or saline was administered intraperitoneally immediately after and at the 12th hour of the burn injury. Rats were decapitated 24 h after burn injury and the skin samples, as well as tissue samples from stomach, ileum and colon, were taken for the determination of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity and collagen contents. Tissues were also examined microscopically. Tumor necrosis factor-alpha (TNF-alpha) and lactate dehydrogenase (LDH) were assayed in serum samples. Severe skin scald injury (30% of total body surface area) caused a significant decrease in GSH level, which was accompanied with significant increases in MDA level, MPO activity and collagen content of tissues. Similarly, serum TNF-a and LDH were elevated in the burn 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 thermal trauma. Findings of the present study suggest that montelukast possesses an anti-inflammatory effect on burn-induced gastrointestinal damage and protects against oxidative injury by a neutrophil-dependent mechanism. (c) 2005 Elsevier Ltd. All rights reserved.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 Leukotriene receptor blocker montelukast protects against burn-induced oxidative injury of the skin and remote organs(ELSEVIER SCI LTD, 2005) YEGEN, BERRAK; Sener, G; Kabasakal, L; Cetinel, S; Contuk, G; Gedik, N; Yeken, BCThermal injury elicits several systemic consequences, among them the systemic inflammatory response where the generation of reactive oxygen radicals and lipid peroxidation play important roles. In the present study, we investigated whether the leukotriene receptor blocker montelukast is protective against burn-induced remote organ injury. Under brief ether anaesthesia, shaved dorsum of the rats was exposed to 90 degrees C (burn group) or 25 degrees C (control group) water bath for 10 s. Montelukast (10 mg/kg) or saline was administered intraperitoneally immediately after and at the 12th hour of the burn injury. Rats were decapitated 24 h after burn injury and the tissue samples from lung, liver, kidney and skin were taken for the determination of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity and collagen contents. Tissues were also examined microscopically. Serum aspartate aminotransferase (AST), alanine aminotransferase (ALT) levels and creatinine, urea (BUN) concentrations were determined to assess liver and kidney function, respectively. Tumor necrosis factor-alpha (TNF-alpha) and lactate dehydrogenase (LDH) were also assayed in serum samples. Severe skin scald injury (30% of total body surface area) caused a significant decrease in GSH level, which was accompanied with significant increases in MDA level, MPO activity and collagen content of tissues. Similarly, serum ALT, AST and BUN levels, as well as LDH and TNF-alpha, were elevated in the burn 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 thermal trauma. Findings of the present study suggest that montelukast possesses an anti-inflammatory effect on burn-induced damage in remote organs and protects against oxidative organ damage by a neutrophil-dependent mechanism. (C) 2005 Elsevier Ltd and ISBI. 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 Role of Melatonin and Luzindole in Rat Mammary Cancer(TAYLOR & FRANCIS INC, 2012) YEGEN, BERRAK; Umit, Ugurlu M.; Berna, Terzioglu; Handan, Kaya; Ipek, Erbarut; Berrak, Yegen; Can, Erzik; Bahadir, Gulluoglu M.Background: Recent studies have analyzed the efficacy of various agents in experimental chemoprevention trials. In our study, the effects of melatonin (Mel) and its antagonist Luzindole (Luz) on Heme oxygenase-1 (HO-1) in a NMU (N-methyl-N-nitrosourea)-induced rat mammary carcinoma model are investigated. We aim to demonstrate the relationship between Mel and HO-1. Methods: Spraque-Dawley rats were treated with NMU at age 55 days to induce mammary carcinoma. Forty-eight rats were divided into four groups consisting of: (a) physiological saline group (PSG); (b) control group, NMU is given; (c) Mel group (500 mu g daily); (d) Mel antagonist Luz group (0.25 mg/kg/day i.p.). The animals were sacrificed; their serum and tissues were sampled for histopathologic evaluation, markers of endocrine derangement (serum prolactin, estradiol, and progesterone levels), apoptotic changes, DNA fragmentation, markers of oxidative stress and HO-1 immune expression were measured. Results: Most tumors developed in the Luz group (42%), followed by the control group (33%), and the Mel group (17%). The tumor latency was longer in Mel-treated group (control and Luz at week 17, Mel at week 21). The maximum tumor volume was also smaller in Mel group when compared to control and Luz groups (p < .05). In Mel group estradiol, progesterone, and prolactin levels were decreased compared to control group (p < .001; p < .01; and p < .01) and levels of apoptotic activity and DNA fragmentation ratio increased. Conclusions: The increment of HO-1 expression with Mel is described; possible underlying mechanisms of these effects await further investigations.Publication Metadata only Anti-inflammatory effect of acute stress on experimental colitis is mediated by cholecystokinin-B receptors(PERGAMON-ELSEVIER SCIENCE LTD, 2004) YEGEN, BERRAK; Gulpinar, MA; Ozbeyli, D; Arbak, S; Yegen, BCWe aimed to investigate the effects of electric shock (ES) on the course of experimental colitis and the involvement of possible central and peripheral mechanisms. In Sprague-Dawley rats (n = 190) colitis was induced by intracolonic administration 2,4,6-trinitrobenzenesulfonic acid (TNBS). The effects of ES (0.3-0.5 mA) or the central administration of corticotropin-releasing factor (CRF; astressin, 10 mug/kg) or cholecystokinin (CCKB; 20 mug/kg) receptor antagonists and peripheral glucocorticoid receptor (RU-486; 10 mg/kg) or ganglion (hexamethonium; 15 mg/kg) blockers on TNBS-induced colitis were studied by the assessment of macroscopic score, histological analysis and tissue myeloperoxidase activity. ES reduced all colonic damage scores (p < 0.05-0.01), while central CRF (p < 0.05-0.001) and CCKB receptor (p < 0.05-0.01) blockers or peripheral hexamethonium (p < 0.05-0.01) and RU-486 (p < 0,05) reversed stress-induced improvement. ES demonstrated an anti-inflammatory effect on colitis, which appears to be mediated by central CRF and CCK receptors with, the participation of hypothalamo-pituitary-adrenal axis and the sympathetic nervous system. (C) 2004 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 L-Carnitine ameliorates methotrexate-induced oxidative organ injury and inhibits leukocyte death(SPRINGER, 2006) YEGEN, BERRAK; Sener, G; Eksioglu-Demiralp, E; Cetiner, M; Ercan, F; Sirvanci, S; Gedik, N; Yegen, BCMethotrexate (MTX), a folic acid antagonist widely used for the treatment of a variety of tumors and inflammatory diseases, affects normal tissues that have a high rate of proliferation, including the hematopoietic cells of the bone marrow and the gastrointestinal mucosal cells. To elucidate the role of free radicals and leukocytes in MTX-induced oxidative organ damage and the putative protective effect of L-carnitine (L-Car), Wistar albino rats were administered a single dose of MTX (20 mg/kg) followed by either saline or L-Car (500 mg/kg) for 5 days. After decapitation of the rats, trunk blood was obtained, and the ileum, liver, and kidney were removed for histological examination and for the measurement of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity, and collagen content. Our results showed that MTX administration increased the MDA and MPO activities and collagen content and decreased GSH levels in all tissues, while these alterations were reversed in L-Car-treated group. The elevated serum TNF-alpha level observed following MTX treatment was depressed with L-Car. The oxidative burst of neutrophils stimulated by Annexin V was reduced in the saline-treated MTX group, while L-Car abolished this inhibition. Similarly, flow cytometric measurements revealed that leukocyte apoptosis was increased in MTX-treated animals, while L-Car reversed these effects. Severe degeneration of the intestinal mucosa, liver parenchyma, and glomerular and tubular epithelium observed in the saline-treated MTX group was improved by L-Car treatment. These results suggest that L-Car, possibly via its free radical scavenging and antioxidant properties, ameliorates MTX-induced oxidative organ injury and inhibits leukocyte apoptosis. Thus, supplementation with L-Carnitine as an adjuvant therapy may be promising in alleviating the systemic side-effects of chemotherapeutics.