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 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 Open Access Cerrahi menopoz oluşturulmuş sıçanların karaciğer ve böbrek dokularında oksidan/antioksidan dengenin korunmasında egzersizin ve östrojenin yararlı etkileri(2022-09-01) YÜKSEL, MERAL; ERCAN, FERİHA; YILDIRIM, ALPER; YEGEN, BERRAK; Tamer S. A. , Levent N., Yüksel M., Ercan F., Yıldırım A., Yegen B.Amaç: Bu çalışmanın amacı cerrahi olarak menopoz oluşturulan sıçanların böbrek ve karaciğerlerinde gözlenen histopatolojik ve fonksiyonel değişiklikleri ve östrojen veya egzersizin ya da östrojen-egzersiz kombinasyonunun oksidan hasar üzerine etkilerini araştırmaktır.Materyal ve Metot: Anestezi altında Sprague Dawley dişi sıçanlara (n=32) bilateral overiektomi uygulandı ve tüm sıçanlar rastgele olarak iki gruba ayrıldı. Sıçanların yarısına normal içme suyu, diğer yarısının içme sularına östrojen (1mg/kg/gün) eklendi. İki hafta sonra gruplar kendi içlerinde sedanter ve egzersiz (5 gün/hafta, 30 daki-ka, 8 hafta) gruplarına ayrıldı. Deney protokolünün sonun-da serum, karaciğer ve böbrek örnekleri biyokimyasal ve histopatolojik incelemeler için alındı. Femurda da histopa-tolojik değerlendirme yapıldı.Bulgular: Cerrahi olarak menopoz oluşturulan sıçan-larda östrojenin böbrek dokusunda nötrofil infiltrasyonunu ve reaktif oksijen türlerinin üretimini baskılayarak koruyu-cu etki gösterdiği, kemik kütlesinde hafif düzeyde artışa neden olduğu, ancak karaciğerin antioksidan glutatyon düzeyinde azalmaya yol açtığı belirlenmiştir. Buna karşın, östrojen uygulaması menopozda yapılan egzersiz nedeniy-le karaciğerde oluşan oksidan stresi engellemiştir. Egzer-sizle veya egzersize östrojen tedavisinin eklenmesiyle böbrek fonksiyonları önemli ölçüde etkilenmezken, kemik yapısında tek başına östrojene kıyasla daha olumlu deği-şiklikler gözlenmiştir.Sonuç: Östrojen replasmanı kemik dokusundaki olum-lu etkilerinin yanı sıra karaciğer ve böbrekte oksidan stresi azaltmakta ve özellikle karaciğerde egzersize bağlı gelişen oksidan stresi baskılayarak koruyucu etki göstermektedir.Publication Metadata only 83: phoenixin-14 ameliorates cholestatic liver injury and bileinduced acute pancreatic injury in rats(2022-05-01) KAHRAMAN, MERVE MERİÇ; YÜKSEL, MERAL; YEGEN, BERRAK; ERCAN, FERİHA; Şen L. S. , Kahraman M. M. , Mermer K. S. , Köroğlu K., Yüksel M., İmeryüz N., Ercan F., Yegen B.Background: Bile duct obstruction, which results in cholestatic liver injury, is also the major cause of acute pancreatitis. Phoenixin (PNX) was originally defined as a hypothalamic peptide associated with a wide range of physiological processes and exerts antioxidant and antiinflammatory effects. PNX is expressed in several peripheral organs including pancreas and liver. We aimed to evaluate possible therapeutic effects of PNX on hepatic and pancreatic damage induced by biliary or pancreaticobiliary duct obstruction. Methods: In male Sprague Dawley rats, bile duct ligation (BDL; n=16) or pancreaticobiliary duct ligation (PBDL; n= 16) was performed under ketamine anesthesia, while control rats (n=8) had sham-surgery. Either PNX-14 (50 µg/kg/day) or saline was subcutaneously injected immediately after surgery and in the following 2 days. On the post-operative 3rd day, hepatic and renal blood flow was measured using laser Doppler flowmeter under anesthesia and the rats were then euthanized. In the liver and pancreas samples, levels of malondialdehyde, antioxidant glutathione and myeloperoxidase activity were measured by spectrophotometry, while luminol- and lucigenin-enhanced chemiluminescence (CL) levels were measured to assess formation of reactive oxygen species (ROS). Tissue samples were stained by hematoxylin-eosin to calculate microscopic damage scores. Statistical analyses were made by one-way ANOVA. Results: Increased microscopic damage scores in the pancreas of saline-treated PBDL (p<0.001) and in the liver of saline-treated BDL group (p<0.001) were reduced by PNX14 treatment (p<0.01), but PBDL-induced hepatic damage (p<0.001) was not changed by PNX-14. Pancreatic and hepatic levels of malondialdehyde and myeloperoxidase activity and pancreatic glutathione levels were not different among the experimental groups, while hepatic glutathione level was elevated in PNX-14-treated BDL (p<0.001) and PBDL (p<0.01) groups as compared to control group. Despite a non-significant fall in renal or hepatic blood flow in saline-treated BDL rats, PBDL significantly reduced hepatic (p<0.001) and renal (p<0.01) blood flow, while PNX-14 reversed blood flow in both organs back to control levels (p<0.05). The CL levels of luminol and lucigenin were increased in both hepatic and pancreatic tissues of saline-treated BDL and PBDL groups (p<0.05-0.001), showing enhanced ROS generation. However, CL levels in both the liver and pancreas of PNX-14-treated BDL and PBDL groups were significantly reduced as compared to those measured in the liver and pancreas of respective saline-treated groups (p<0.05-0.001). Conclusion: In conclusion, cholestatic liver injury and bile-induced pancreatic injury are alleviated by PNX-14 treatment, which appears to act via its ROS scavenging activity, by replenishing hepatic antioxidant capacity and restoring impaired organ perfusion.Publication Metadata only Halofuginone, a Specific Inhibitor of Collagen Type 1 Synthesis, Ameliorates Oxidant Colonic Damage in Rats with Experimental Colitis(SPRINGER, 2010) YEGEN, BERRAK; Karakoyun, Berna; Yuksel, Meral; Ercan, Feriha; Salva, Emine; Isik, Isil; Yegen, Berrak C.To evaluate the effect of halofuginone on trinitrobenzene sulfonic acid (TNBS)-induced colonic injury, rats were given halofuginone (40 mu g/kg, intraperitoneally) or saline 1 h before the induction of colitis, and the injections were continued twice daily for 3 days until they were decapitated. High macroscopic and microscopic damage scores, elevated colonic wet weights, colonic myeloperoxidase activity, malondialdehyde and tissue collagen level, and luminol chemiluminescence values, and marked reduction in glutathione level of the saline-treated colitis group were all reversed by treatment with halofuginone. In conclusion, halofuginone exerts beneficial effects in TNBS-induced colonic inflammation in rats. The anti-inflammatory effects of halofuginone appear to involve suppression of neutrophil accumulation, preservation of endogenous glutathione, and inhibition of reactive oxidant generation. Halofuginone also shows antifibrotic effect via inhibition of tissue collagen production. The present data encourage possible use of the antifibrotic halofuginone as an anti-inflammatory agent in improving oxidative injury in colitis.Publication Metadata only Stimulation of estrogen receptors attenuates oxidant skin injury in hyperglycemic rats with incisional wound(2023-01-01) KAHRAMAN, MERVE MERİÇ; YÜKSEL, MERAL; ERCAN, FERİHA; YEGEN, BERRAK; Sen L. S., Akgun T., KAHRAMAN M. M., YÜKSEL M., ERCAN F., YEGEN B.Publication Open Access High-fat Diet Enhances Gastric Contractility, but Abolishes Nesfatin-1-induced Inhibition of Gastric Emptying(KOREAN SOC NEUROGASTROENTEROLOGY & MOTILITY, 2021-04-30) YEGEN, BERRAK; Ozdemir-Kumral, Zarife N.; Koyuncuoglu, Turkan; Arabaci-Tamer, Sevil; Cilingir-Kaya, Ozlem T.; Koroglu, Ayca K.; Yuksel, Meral; Yegen, Berrak C.Neither HFD nor NES-1 changed methylcellulose emptying, but NES-1 delayed saline emptying in cannulated ND-rats. Inhibitory effect of NES-1 on gastric emptying in ND-rats was reversed by all antagonists, and abolished in HFD-rats. In HFD-rats, carbachol-induced contractility was enhanced in gastric, but inhibited in ileal strips. HFD increased body weight, while serum triglycerides, alanine transaminase, aspartate aminotransferase, glucose, and levels of malondialdehyde, glutathione, myeloperoxidase activity, and luminolchemiluminescence in hepatic, ileal, and adipose tissues were similar in ND- and HFD-rats, but only lucigenin-chemiluminescence was Background/Aims Gastrointestinal motility changes contribute to development and maintenance of obesity. Nesfatin-1 (NES-1) is involved in central appetite control. The aim is to elucidate effects of NES-1 and high-fat diet (HFD) on gastrointestinal motility and to explore myenteric neuron expressions of tyrosine hydroxylase (TH), vasoactive intestinal peptide (VIP), and neuronal nitric oxide synthase (nNOS) in HFDinduced oxidative injury. Methods Sprague-Dawley rats were fed with normal diet (ND) or HFD. Gastric emptying rate was measured following NES-1 (5 pmol/rat, intracerebroventricular) preceded by subcutaneous injections of glucagon-like peptide 1 (GLP-1), cholecystokinin 1 (CCK-1), and gastrin/CCK-2 receptor antagonists. In carbachol-contracted gastric and ileal strips, contractile changes were recorded by adding NES1 (0.3 nmol/L), GLP-1, CCK-1, and gastrin/CCK-2 antagonists. Results Neither HFD nor NES-1 changed methylcellulose emptying, but NES-1 delayed saline emptying in cannulated ND-rats. Inhibitory effect of NES-1 on gastric emptying in ND-rats was reversed by all antagonists, and abolished in HFD-rats. In HFD-rats, carbachol-induced contractility was enhanced in gastric, but inhibited in ileal strips. HFD increased body weight, while serum triglycerides, alanine transaminase, aspartate aminotransferase, glucose, and levels of malondialdehyde, glutathione, myeloperoxidase activity, and luminolchemiluminescence in hepatic, ileal, and adipose tissues were similar in ND-and HFD-rats, but only lucigenin-chemiluminescence was increased in HFD-rats. Vasoactive intestinal peptide (VIP) and TH immunoreactivities were depressed and nNOS immunoreactivity was increased in gastric tissues of HFD-rats, while VIP and TH were enhanced, but nNOS was reduced in their intestines. Conclusions HFD caused mild systemic inflammation, disrupted enteric innervation, enhanced gastric contractility, inhibited ileal contractility, and eliminated inhibitory effect of NES-1 on gastric motility. (J Neurogastroenterol Motil 2021;27:265-278)Publication Metadata only Halofuginone improves caustic-induced oxidative injury of esophagus in rats(SPRINGER JAPAN KK, 2018) YEGEN, BERRAK; Cerit, Kivilcim Karadeniz; Karakoyun, Berna; Bahadir, Elif; Yuksel, Meral; Bulbul, Nurdan; Ercan, Feriha; Dagli, E. Tolga; Yegen, Berrak C.The aim of this study is to evaluate the anti-inflammatory and anti-fibrotic effects of halofuginone in caustic esophageal burn injury in rats. Corrosive esophageal injury (CEI) was produced in male Wistar albino rats by instilling NaOH solution (1 ml, 37.5%) into the distal esophagus. Rats were decapitated on the 3rd day (early group) or 28th day (late group), and treated daily with either saline or halofuginone (100 A mu g/kg/day; i.p.), continued on alternate days after the third day. Histopathological evaluation and measurement of nitric oxide (NO), peroxynitrite (ONOO-) and oxygen-derived radicals by chemiluminescence (CL) were made in the distal 2 cm of the esophagus. Non-irrigated proximal esophageal samples were assessed for the levels of nuclear factor (NF)-kappa B, caspase-3, glutathione (GSH), malondialdehyde (MDA) and myeloperoxidase (MPO) activity. GSH, MDA, NF-kappa B and caspase-3 levels, and MPO activity in the proximal esophagus were not different among groups. Increased number of TUNEL (+) cells in the irrigated esophagus of the early and late caustic injury groups was reduced by halofuginone treatment. High microscopic damage scores in both early and late CEI groups were decreased with halofuginone treatment. NO, ONOO- and CL levels, which were elevated in the saline-treated early CEI group, were reduced by halofuginone treatment, but reduced NO and ONOO- levels in the late period of saline-treated group were increased by halofuginone. In addition to its anti-fibrotic effects, current findings demonstrate that halofuginone exerts antioxidant and anti-apoptotic actions and supports therapeutic potential for halofuginone in CEI-induced oxidative stress.Publication Metadata only Alpha Lipoic Acid Alleviates Oxidative Stress and Preserves Blood Brain Permeability in Rats with Subarachnoid Hemorrhage(SPRINGER/PLENUM PUBLISHERS, 2010) YEGEN, BERRAK; Ersahin, Mehmet; Toklu, Hale Z.; Cetinel, Sule; Yuksel, Meral; Erzik, Can; Berkman, M. Zafer; Yegen, Berrak C.; Sener, GoekselThe neuroprotective effect of alpha lipoic acid (ALA; 100 mg/kg, po), a dithiol antioxidant, on experimentally induced subarachnoid hemorrhage (SAH) was assessed in Wistar albino rats. Neurological examination scores recorded at the 48th h of SAH induction were increased in SAH groups, which were accompanied with significant increases in the formation of reactive oxygen species, DNA fragmentation ratios, malondialdehyde levels and myeloperoxidase activity, while significant decreases in the brain glutathione content and Na+, K+-ATPase activity were observed. On the other hand, ALA treatment reversed all these biochemical indices as well as SAH-induced histopathological alterations. Increased brain edema, impaired blood-brain-barrier permeability and neurological scores were also improved by ALA treatment. The results demonstrate that ALA exerts neuroprotective effects via the enhancement of endogenous antioxidant enzyme activity, the inhibition of neutrophil accumulation and free radical generation, suggesting a therapeutic potential in reducing secondary injury after SAH in patients.Publication Metadata only The effects of Nigella sativa against oxidative injury in a rat model of subarachnoid hemorrhage(SPRINGER WIEN, 2011) YEGEN, BERRAK; Ersahin, Mehmet; Toklu, Hale Z.; Akakin, Dilek; Yuksel, Meral; Yegen, Berrak C.; Sener, GokselThe aim of the study was to investigate the putative neuroprotective effect of Nigella sativa oil (NSO) treatment against subarachnoid hemorrhage (SAH) in rats. To induce SAH, rats were injected with 0.3 ml blood into their cisterna magna. Male Wistar albino rats were divided as control, vehicle-treated SAH, and NSO-treated (0.2 ml/kg, intraperitoneally) SAH groups. Forty-eight hours after SAH induction, neurological examination scores were recorded and the rats were decapitated. Brain tissue samples were taken for blood brain barrier permeability, brain water content, or determination of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO), and Na+-K+-ATPase activities. On the second day of SAH induction, neurological examination scores were increased in SAH groups, while SAH caused significant decreases in brain GSH content and Na+-K+-ATPase activity, which were accompanied with significant increases in MDA levels and MPO activity. The histological observation showed vasospasm of the basillary artery. On the other hand, NSO treatment markedly improved the neurological scores while all oxidant responses were prevented, implicating that NSO treatment may be of therapeutic use in preventing oxidative stress due to SAH.
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