Person: ŞİRVANCI, SERAP
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ŞİRVANCI
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SERAP
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Publication Metadata only The neuroprotective and anti-apoptotic effects of melatonin on hemolytic hyperbilirubinemia-induced oxidative brain damage(WILEY, 2016) MEMİŞOĞLU, ASLI; Pazar, Asilay; Kolgazi, Meltem; Memisoglu, Asli; Bahadir, Elif; Sirvanci, Serap; Yaman, Akan; Yegen, Berrak C.; Ozek, ErenMelatonin exerts protection in several inflammatory and neurodegenerative disorders. To investigate the neuroprotective effects of melatonin in an experimental hemolysis-induced hyperbilirubinemia, newborn Sprague-Dawley rats (25-40 g, n = 72) were injected with phenylhydrazine hydrochloride (PHZ; 75 mg/kg) and the injections were repeated at the 24th hour. Rats were treated with saline or melatonin (10 mg/kg) 30 min before the first and second PHZ injections and 24 h after the 2nd PHZ injections. Control rats (n = 24) were injected with saline, but not PHZ. At sixth hours after the last injections of saline or melatonin, all rats were decapitated. Tumor necrosis factor (TNF)-alpha, IL-1 beta, IL-10 and brain-derived neurotrophic factor (BDNF) and S100B levels in the plasma were measured. Brain tissue malondialdehyde (MDA), glutathione (GSH) levels and myeloperoxidase (MPO) activities were measured, and brain tissues were evaluated for apoptosis by TUNEL method. In the saline-treated PHZ group, hemoglobin, hematocrit levels were reduced, and total/direct bilirubin levels were elevated when compared to control group. Increased plasma TNF-alpha, IL-1 beta levels, along with decreased BDNF, S100B and IL-10 values were observed in the saline-treated PHZ group, while these changes were all reversed in the melatonin-treated group. Increased MDA levels and MPO activities in the brain tissues of saline-treated hyperbilirubinemic rats, concomitant with depleted brain GSH stores, were also reversed in the melatonin-treated hyperbilirubinemic rats. Increased TUNEL(+) cells in the hippocampus of saline-treated PHZ group were reduced by melatonin treatment. Melatonin exerts neuroprotective and anti-apoptotic effects on the oxidative neuronal damage of the newborn rats with hemolysis and hyperbilirubinemia.Publication Metadata only Neuroprotective Effect of Erythropoietin on PhenylhydrazineInduced Hemolytic Hyperbilirubinemia in Neonatal Rats(SPRINGER/PLENUM PUBLISHERS, 2017) MEMİŞOĞLU, ASLI; Memisoglu, Asli; Kolgazi, Meltem; Yaman, Akan; Bahadir, Elif; Sirvanci, Serap; Yegen, Berrak C.; Ozek, ErenNeonatal unconjugated hyperbilirubinemia might cause severe bilirubin neurotoxicity in especially hemolytic conditions. The study aimed to elucidate the potential neuroprotective effects of erythropoietin (EPO) in hemolysis-induced hyperbilirubinemia. In newborn rats, hyperbilirubinemia secondary to hemolysis was induced by injecting with phenylhydrazine hydrochloride (PHZ) and rats were injected with either vehicle or EPO. At 54th hour of the PHZ injection, rats were decapitated. Serum levels of TNF-alpha, IL-1 beta, IL-10, brain-derived neurotrophic factor (BDNF) and S100-B and brain malondialdehyde, glutathione levels and myeloperoxidase activities were measured. TUNEL staining and NF-kappa B expression were evaluated. As compared to control pups, in vehicle-treated PHZ group, TNF-alpha and IL- 1 beta levels, malondialdehyde level and myeloperoxidase activity were increased with concomitant decreases in IL-10 and glutathione. All EPO regimens reversed PHZ-induced alterations in IL-10, TNFa, malondialdehyde and glutathione levels. Three-daytreatment abolished increases in myeloperoxidase activity and IL-1 beta levels, while BDNF and S100-B were elevated. Increased TUNEL (+) cells and NF-kappa B expressions in the brain of PHZ group were reduced in the 3-day-treated group. EPO exerted anti- inflammatory effects on PHZinduced neural damage in newborn rats, while the neuroprotection was more obvious when the treatments were repeated successively. The results suggest that EPO treatment may have a therapeutic potential in supporting neuroplasticity in the hyperbilirubinemic neonates.Publication Metadata only The ameliorative effects of melatonin on acetic acid-induced gastric ulcer in rats via its modulatory effects on gut microbiota(CUKUROVA UNIV, FAC MEDICINE, 2021) YILDIRIM, ALPER; Tamer, Sevil Arabaci; Yildirim, Alper; Cevik, Ozge; Aksu, Burak; Yuksel, Meral; Dertsiz, Ekin Kuntsal; Sirvanci, Serap; Yegen, Berrak C.Purpose: The aim of this study was of observe the possible protective effects of melatonin pretreatment on oxidative damage and microbiota alteration due to gastric ulcer in rats. Materials and Methods: Wistar-albino rats were given (n=32) melatonin (4 mg/kg/day), antibiotic mixture (AB; 1g/L ampicillin + 1g/L neomycin + 1g/L metronidazole), melatonin+AB in drinking water for 12 days or tap water for 15 days (control group; n=8). Subsequently, ulcer was induced. All treatments were continued for three days. Gastric tissues were obtained for biochemical and histopathological examinations, and fecal samples from the rectum were stored for bacteriological measurements. Results: MPO and MDA levels were increased in untreated ulcer groups compared to the control group. In addition, the levels of luminol-lucigenin chemiluminescence (CL) and 8-OHdG and TNF-alpha and IL-8 protein expressions were also increased, while TNF-alpha, IL-8, MDA, 8-OHdG, luminol and lucigenin CL levels were significantly decreased in the melatonin-treated ulcer groups. However, melatonin+AB pretreatment increased antioxidant GSH levels and anti-inflammatory IL-10 levels, and suppressed caspase-3 activity and reduced MPO back to control level. Conclusion: We anticipate that melatonin treatment, which is an effective antioxidant and radical scavenger, can accelerate ulcer healing along with antibiotics and increase the variety of bacteria impaired by antibiotics in the colon.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.Publication Metadata only Nesfatin-1 alleviates gastric damage via direct antioxidant mechanisms(ACADEMIC PRESS INC ELSEVIER SCIENCE, 2015) YEGEN, BERRAK; Kolgazi, Meltem; Cantali-Ozturk, Cigdem; Deniz, Rabia; Ozdemir-Kumral, Zarife Nigar; Yuksel, Meral; Sirvanci, Serap; Yegen, Berrak C.Background: Indomethacin is a nonsteroidal anti-inflammatory drug, which is known to produce serious side effects, causing ulcerative lesions. Nesfatin-1, a newly identified anorexigenic peptide, was recently shown to have neuroprotective effects. The aim of the study was to investigate the anti-inflammatory effects of nesfatin-1 on indomethacin-induced gastric ulcer. Materials and methods: After a 24-h starvation period, ulcer was induced in Sprague-Dawley rats by subcutaneous administration of indomethacin (25 mg/kg), whereas control group received vehicle. Fifteen minutes after ulcer induction, rats were treated with either saline or nesfatin-1 (0.1, 0.3, or 1 mu g/kg, intraperitoneally). At the fourth hour, all rats were decapitated and their trunk blood was collected for tumor necrosis factor (TNF)-alpha and interleukin (IL)-6 measurements. Stomach samples were examined microscopically and analyzed for myeloperoxidase (MPO) activity, malondialdehyde (MDA), glutathione (GSH), luminol-, and lucigenin-enhanced chemiluminescence (CL) levels. Results: Ulcer induction increased serum TNF-alpha; and IL-6 levels, gastric CL and MDA levels and MPO activity but decreased gastric GSH content (P < 0.05-0.001). On the other hand, 0.1 mu g/kg dose of nesfatin-1 reduced microscopic and macroscopic damage scores, decreased MPO activity and MDA levels, CL and IL-6 levels, whereas gastric GSH was replenished (P < 0.01). However, indomethacin-induced increase in TNF-alpha level was abolished at only 1 mu g/kg dose of nesfatin-1 (P < 0.01). Conclusions: Nesfatin-1 alleviated indomethacin-induced gastric injury, suggesting that the anti-inflammatory and gastroprotective effects of nesfatin-1 on oxidative gastric damage could be implemented by supporting the balance in oxidant and antioxidant systems while inhibiting the generation of pro-inflammatory mediators. (C) 2015 Elsevier Inc. All rights reserved.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 Nesfatin-1 improves oxidative skin injury in normoglycemic or hyperglycemic rats(ELSEVIER SCIENCE INC, 2016) YEGEN, BERRAK; Solmaz, Ali; Bahadir, Elif; Gulcicek, Osman B.; Yigitbas, Hakan; Celik, Atilla; Karagoz, Ayca; Ozsavci, Derya; Sirvanci, Serap; Yegen, Berrak C.Hyperglycemia is one of the major causes of suppressed angiogenesis and impaired wound healing leading to chronic wounds. Nesfatin-1 a novel peptide was reported to have antioxidant and anti-apoptotic properties. This study is aimed to investigate the potential healing-promoting effects of nesfatin-1 in non diabetic or diabetic rats with surgical wounds. In male Sprague-Dawley rats, hyperglycemia was induced by intraperitoneal (ip) injection of streptozotocin (55 mg/kg). Under anesthesia, dorsum skin tissues of normoglycemic (n = 16) and hyperglycemic rats were excised (2 x 2 cm, full-thickness), while control rats (n = 16) had neither hyperglycemia nor wounds. Half of the rats in each group were treated ip with saline, while the others were treated with nesfatin-1 (2 g/kg/day) for 3 days until they were decapitated. Plasma interleukin-1-beta (IL-1 beta), transforming growth factor-beta (TGF-beta-1), IL-6 levels, and dermal tissue malondialdehyde (MDA), glutathione (GSH) levels, myeloperoxidase (MPO) and caspase-3 activity were measured. For histological examination, paraffin sections were stained with hematoxylin-eosin or Masson's trichrome and immunohistochemistry for vascular endothelial growth factor (VEGF) was applied. ANOVA and Student's t-tests were used for statistical analysis. Compared to control rats, skin MPO activity, MDA and caspase-3 levels were increased similarly in saline-treated normo- and hyperglycemic rats. Nesfatin-1 depressed MDA, caspase-3, MPO activity and IL-1 beta with concomitant elevations in dermal GSH and plasma TGF-beta-1 levels. Histopathological examination revealed regeneration of epidermis, regular arrangement of collagen fibers in the dermis and a decrease in VEGF immunoreactivity in the epidermal keratinocytes of nesfatin-1-treated groups. Nesfatin-1 improved surgical wound healing in both normo- and hyperglycemic rats via the suppression of neutrophil recruitment, apoptosis and VEGF activation. (C) 2016 Elsevier Inc. All rights reserved.Publication Metadata only Aqueous garlic extract alleviates ischaemia-reperfusion-induced oxidative hepatic injury in rats(ROYAL PHARMACEUTICAL SOC GREAT BRITAIN, 2005) YEGEN, BERRAK; Sener, G; Sehirli, O; Ipci, Y; Ercan, F; Sirvanci, S; Gedik, N; Yegen, BCThis study was designed to examine the effects of aqueous garlic extract (AGE) on hepatic ischaemia-reperfusion (I/R) injury in rats. For this purpose, Wistar albino rats were subjected to 45min of hepatic ischaemia, followed by a 60-min reperfusion period. AGE (1 mL kg(-1), i.p., corresponding to 500 mg kg(-1)) or saline was administered twice, 15 min before ischaemia and immediately before the reperfusion period. Serum aspartate aminotransferase (AST) and alanine aminotransferase.(ALT) levels were determined to assess liver functions. Liver tissues were taken for the determination of malondialdehyde (MDA) levels, an end product of lipid peroxidation; glutahione (GSP.) levels, a key antioxidant; and myeloperoxidase (MPO) activity, as an indirect index of neutrophil inifiltration Hepatic collagen content, as a fibrosis marker, was also determined. Plasma ALT and AST activities, were elevated in the I/R group as compared with the control group, while these increases significantly decreased by AGE treatment. Hepatic GSH levels, significantly, depressed by I/R were elevated back to control levels in the AGE-treated I/R group. Increases in tissue MDA levels and MPO activity due to I/R injury were reduced back to control levels by AGE treatment. Similarly,, increased hepatic collagen content in the I/R group was reduced to the control level with AGE treatment. Since AGE administration alleviated the I/R-incluced injury of the liver and improved the hepatic and function, it seems likely that AGE, with its antioxidant and oxidant-scavenging properties, may be of potential therapeutic value in protecting the liver against oxidative injury due to ischaemia-reperfusion.