Person: YEGEN, BERRAK
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YEGEN
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BERRAK
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Publication Metadata only The antifibrotic drug halofuginone reduces ischemia/reperfusion-induced oxidative renal damage in rats(ELSEVIER SCI LTD, 2013) YEGEN, BERRAK; Cerit, Kivilcim Karadeniz; Karakoyun, Berna; Yuksel, Meral; Ozkan, Naziye; Cetinel, Sule; Dagli, E. Tolga; Yegen, Berrak C.; Tugtepe, HalilAim: The objective of the present study was to evaluate the protective effects of halofuginone against renal ischemia/reperfusion (I/R) injury. Materials and methods: Male Wistar albino rats were unilaterally nephrectomized and the left renal pedicles were occluded for 45 min to induce ischemia and then reperfused for 6 h (early) or for 72 h (late). The rats were treated intraperitoneally with either halofuginone (100 mu g/kg/day) or saline 30 min prior to ischemia and the dose was repeated in the late reperfusion groups. In the sham groups, rats underwent unilateral nephrectomy and were treated at similar time points. The animals were decapitated at either 6 h or 72 h of reperfusion and trunk blood and kidney samples were obtained. Results: I/R injury increased renal malondialdehyde levels, myeloperoxidase activity and reactive oxygen radical levels, and decreased the renal glutathione content. Halofuginone treatment was found to reduce oxidative I/R injury and improve renal function in the rat kidney, as evidenced by reduced generation of reactive oxygen species, depressed lipid peroxidation and myeloperoxidase activity, and increased glutathione levels. Conclusions: The present findings demonstrate the anti-inflammatory and antioxidant effects of halofuginone in renal I/R injury, supporting its potential use where renal I/R injury is inevitable. (C) 2012 Journal of Pediatric Urology Company. Published by Elsevier Ltd. All rights reserved.Publication Metadata only Melatonin supports alendronate in preserving bone matrix and prevents gastric inflammation in ovariectomized rats(WILEY, 2019) YEGEN, BERRAK; Gurler, Esra Bihter; Cilingir-Kaya, Ozlem Tugce; Eyuboglu, Irem Peker; Ercan, Feriha; Akkiprik, Mustafa; Reiter, Russell J.; Yegen, Berrak C.The anti-catabolic bisphosphonate alendronate is considered as the first-line medical treatment in post-menopausal osteoporosis; but several side effects, including gastric mucosal injury, are associated with its use. The aim was to elucidate whether combined treatment with melatonin plus alendronate would be more advantageous in the maintenance of bone and the prevention of gastric side effects. Under anaesthesia, female Sprague-Dawley rats underwent bilateral ovariectomy (OVX), while control group had sham surgery. Four weeks after the surgery, OVX rats were treated with saline, melatonin (25 mu g/mL/d), alendronate (70 mu g/kg/wk), melatonin + alendronate, melatonin + melatonin receptor antagonist (luzindole, 10 mu g/kg/d) or alendronate + melatonin + luzindole for 8 weeks. Rats were euthanized at the end of 12th week. Runx2 expression, apoptotic cells, and trabecular thickness were evaluated in tibiae, while gastric tissues were analysed for oxidative injury parameters. In all OVX groups, Runx2 expression was depressed. Saline-treated OVX group presented an extreme decrease in calcified area in opposition to melatonin- or alendronate-treated groups, while the bones in alendronate + melatonin-treated group were similar to those of the sham-operated group. Concomitant with the improvements examined histologically in bone tissues, quantitative TUNEL (+) cells were similarly lower in alendronate- or melatonin-treated groups. Oxidative gastric damage was increased in saline- or alendronate-treated groups, which were depressed in the presence of melatonin. Although melatonin and alendronate exerted similar supportive effects on the maintenance of bone mass, melatonin may have a more advantageous impact by protecting against OVX-induced gastric injury, which was aggravated by alendronate use. Highlights Our results demonstrate that alendronate and melatonin had similar supportive effects on the maintenance of bone mass, while melatonin prevented the gastric side effects of alendronate, making this combination an advisable therapeutic approach in the treatment of menopausal osteoporosis.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 Deneysel sepsis modelinde akut kardiyopulmoner ve serebral hasarda nöropeptit W'nin etkisi(2019-12-13) ATICI, ALİ EMRE; PEKER EYÜBOĞLU, İREM; YEGEN, BERRAK; AKKİPRİK, MUSTAFA; ERCAN, FERİHA; ATICI A. E., ARABACI TAMER S., levent h. n., PEKER EYÜBOĞLU İ., ERCAN F., AKKİPRİK M., YEGEN B.Giriş ve Amaç: Ciddi enfeksiyonların neden olduğu sepsis ve beraberinde görülen çoklu organ yetmezliği, yüksek morbidite ve mortalite oranıyla en önemli klinik sendromlardan biridir. Yakın zamanda tanımlanan ve nöroendokrin düzenlemelerde işlev gördüğü gösterilen nöropeptit W (NPW)’nin, deneysel sepsis modeli oluşturularak akciğer, kalp ve beyin dokularında indüklenen oksidatif hasarda olası tedavi edici etkilerini araştırmayı amaçladık. Yöntemler: Ketamin anestezisi altında, Sprague-Dawley erkek sıçanlarda sham-operasyon (n=8) yapıldı veya çekal ligasyon ve perforasyon ile sepsis oluşturuldu (n=64). Post-operatif ciltaltına 3 doz (hemen sonra, 12. ve 24. saatlerde) serum fizyolojik (SF) veya TNF-alfa inhibitörü + antibiyotik (1 mg/kg etanersept + 100 mg/kg seftriakson) veya NPW (0,1; 0,3; 1, 3 ve 10 g/kg) uygulanırken, sham-opere gruba SF enjeksiyonları yapıldı. Yirmibeşinci saatte alınan kan örneklerinde C-reaktif protein (CRP), kortikosteron ve IL-6 düzeyleri ile çıkarılan akciğer, kalp ve beyin dokularında antioksidan glutatyon, lipit peroksidasyonunu gösteren malondialdehit ile nükleer faktör kappa-B (NF- B) mRNA ekspresyon düzeyleri ölçüldü. Hematoksilen-eozin ile histopatolojik değerlendirmeler yapıldı. Verilerin analizinde ANOVA ve Student’ın t-testleri kullanıldı. Bulgular: Etanersept+antibiyotik veya NPW (1-10 g/kg) tedavili sepsis gruplarında IL6, kortikosteron ve CRP düzeyleri SF-tedavili sepsis grubuna göre düşük bulundu (p<0,05-0,001). SFsepsis grubunda beyinde ve akciğerde malondialdehit düzeylerinin arttığı (p<0,01) ve glutatyonun düştüğü (p<0,01) gözlendi. Etanersept+antibiyotik tedavisi veya NPW beyindeki bu değişiklikleri engelledi (p<0,05-0,001). Buna karşın, akciğerde sepsisle artan malondialdehit ve azalan glutatyon düzeylerine antibiyotik+etanersept etkili olmazken, NPW (0,1-0,3 g/kg) akciğerde malondialdehit düzeyini düşürdü (p<0,05-0,01). Kalp dokusunda ölçülen malondialdehit ve glutatyon düzeyleri ile tüm dokularda ölçülen NF- B ekspresyonları açısından gruplar arasında anlamlı fark bulunmadı. SF-tedavili sepsis grubunda gözlenen dejenere nöron sayısında artış, akciğerde şiddetli kanama, alveoler yapıda bozulma ve nötrofil infiltrasyonu ile kardiyomiyositlerdeki konjesyon ve orta derecede hasar gibi değişikliklerin etanersept+antibiyotik ve NPW (10 g/kg) ile hafiflediği ve histolojik yapıların neredeyse normale döndüğü izlendi. Sonuç: Sepsisin ilk 24 saatinde uygulanan NPW, doza bağımlı olarak akciğer ve beyinde oksidatif hasara karşı koruyucu etki göstermektedir.Publication Metadata only Nesfatin-1 ameliorates oxidative bowel injury in rats with necrotizing enterocolitis: The role of the microbiota composition and claudin-3 expression(W B SAUNDERS CO-ELSEVIER INC, 2020) YEGEN, BERRAK; Cerit, Kivilcim Karadeniz; Koyuncuoglu, Turkan; Yagmur, Damla; Eyuboglu, Irem Peker; Sirvanci, Serap; Akkiprik, Mustafa; Aksu, Burak; Dagli, E. Tolga; Yegen, Berrak C.Background and Purpose: Ongoing high mortality due to necrotizing enterocolitis (NEC) necessitates the investigation of novel treatments to improve the outcome of the affected newborns. The aim was to elucidate the potential therapeutic impact of the nesfatin-1, a peptide with anti-inflammatory and anti-apoptotic effects in several inflammatory processes, on NEC-induced newborn rats. Materials and Methods: Sprague-Dawley pups were separated from their mothers, fed with a hyperosmolar formula and exposed to hypoxia, while control pups had no intervention. NEC-induced pups received saline or nesfatin-1 (0.2 mu g/kg/day) for 3 days, while some nesfatin-1 treated pups were injected with capsaicin (50 mu g/g) for the chemical ablation of afferent neurons. On the 4th day, clinical state and macroscopic gut assessments were made. In intestines, immunohistochemical staining of cycloxygenase-2 (COX-2), nuclear factor (NF)-kappa B-p65 (RelA), vascular endothelial growth factor (VEGF), claudin-3 and zonula occludens-1 (ZO-1) were performed, while gene expressions of COX-2, occludin, claudin-3, NF-kappa B-p65 (RelA) and VEGF were determined using q-PCR. In fecal samples, relative abundance of bacteria was quantified by q-PCR. Biochemical evaluation of oxidant/antioxidant parameters was performed in both intestinal and cerebral tissues. Results: Claudin-3 and ZO-1 immunoreactivity scores were significantly elevated in the nesfatin-1 treated control pups. Nesfatin-1 reduced NEC-induced high macroscopic and clinical scores, inhibited NF-kappa B-65 pathway and maintained the balance of oxidant/antioxidant systems. NEC increased the abundance of Proteobacteria with a concomitant reduction in Actinobacteria and Bacteroidetes, while nesfatin-1 treatment reversed these alterations. Modulatory effects of nesfatin-1 on microbiota and oxidative injury were partially reversed by capsaicin. Immunohistochemistry demonstrated that nesfatin-1 abolished NEC-induced reduction in claudin-3. Gene expressions of COX-2, NF-kappa B, occludin and claudin-3 were elevated in saline-treated NEC pups, while these up-regulated mRNA levels were not further altered in nesfatin-1-treated NEC pups. Conclusion: Nesfatin-1 could be regarded as a potential preventive agent for the treatment of NEC. (C) 2020 Elsevier Inc. All rights reserved.Publication Metadata only Nesfatin-1 treatment preserves antioxidant status and attenuates renal fibrosis in rats with unilateral ureteral obstruction(2022-06-01) ÇETİNEL, ŞULE; YEGEN, BERRAK; KAYA, ÖZLEM TUĞÇE; ÖZBEYLİ, DİLEK; Tezcan N., Özdemir-Kumral Z. N., Yenal N. Ö., Çilingir-Kaya Ö. T., Virlan A. T., Özbeyli D., Çetinel Ş., Yeğen B., Koç M.Background Nesfatin-1 (NES-1), an anorexigenic peptide, was reported to have anti-inflammatory and anti-apoptotic actions in several inflammation models. Methods To elucidate potential renoprotective effects of NES-1, unilateral ureteral obstruction (UUO) was induced in male Sprague Dawley rats by ligating left ureters. The rats were injected intraperitoneally with either saline (SL) or NES-1 (10 mu g/kg/day) for 7 or 14 days (n = 8 in each group). On the 7th or 14th day, obstructed kidneys were removed for the isolation of leucocytes for flow-cytometric analysis and the assessments of biochemical and histopathological changes. Results Opposite to glutathione levels, renal myeloperoxidase activity in the SL-treated UUO group was significantly increased compared with the sham-operated group, while NES-1 treatment abolished the elevation. The percentages of CD8+/CD4+ T-lymphocytes infiltrating the obstructed kidneys were increased in the SL-treated groups but treatment with NES-1 did not prevent lymphocyte infiltration. Elevated tumour necrosis factor-alpha (TNF-alpha) levels in SL-treated UUO group were decreased with NES-1. Although total degeneration scores were similarly increased in all UUO groups, tubular dilatation scores were significantly increased in UUO groups and lowered by NES-1 only in the 7-day treated group. Elevated interstitial fibrosis scores in the SL-treated groups were decreased in both 7- and 14-day NES-1 treated groups, while alpha-smooth muscle actin (alpha-SMA) and apoptosis scores were depressed in both NES-1 treated groups. Conclusion The present data demonstrate that UUO-induced renal fibrosis is ameliorated by NES-1, which appears to involve the inhibition of neutrophil infiltration and thereby amelioration of oxidative stress and inflammation. These data suggest that NES-1 may have a regulatory role in protecting the kidneys against obstruction-induced renal injury.Publication Metadata only Interactions Of Estrogen And Oxytocin Receptors In Colonic Visceral Hypersensitivity Caused By Irritable Bowel Syndrome In Rats(2022-09-01) YILDIRIM, MUSTAFA AKİF; YEGEN, BERRAK; Kahraman M. M. , Mermer K. S. , Aksoy M. B. , Ozden L., Sakalli B. M. , Uludag A., Varol Y., YILDIRIM M. A. , YEGEN B.Publication Metadata only The effect of betulinic acid on TNBS-induced experimental colitis [Betulinik asitin TNBS ile oluşturulan deneysel kolit üzerine etkileri](2013) YEGEN, BERRAK; Şener T.E., Kardaş R.C., Şehirli A.Ö., Ekşioǧlu-Demiral E., Yüksel M., Çetinel Ş., Yeǧen B.C., Şener G.In this study we have investigated the possible protective effect of betulinic acid (BA) on colonic inflammation in rats. Colitis was induced in Sprague-Dawley rats of both sexes by intracolonic administration of 1 ml trinitrobenzene sulphonic acid (TNBS). Colitisinduced rats received orogastrically either betulinic acid (50 mg/kg/day) or vehicle (0.05% DMSO) for 3 days. At the 72nd hour of colitis induction, the rats were decapitated and trunk blood was collected for the measurement of TNF-α, IL-1Β, lactate dehydrogenase (LDH) levels and total antioxidant capacity (AOC). The distal 8 cm of colon were scored macroscopically, and the degree of oxidant damage was evaluated by malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase activity (MPO), collagen content and by histological analysis. Generation of oxidants was evaluated by tissue luminol and lucigenin chemiluminescences (CL). Colitis caused significant increases in the colonic CL values, macroscopic damage scores, MDA, MPO and collagen levels, along with a significant decrease in tissue GSH level. Similarly, serum TNF-α, IL-1Β, as well as LDH were elevated and AOC was reduced in the vehicle-treated colitis group as compared to control group. On the other hand, betulinic acid treatment reversed all these biochemical indices, as well as histopathological alterations induced by TNBS, suggesting that betulinic acid protects the colonic tissue via its radical scavenging and antioxidant activities.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 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.