Person: ÖZDEMİR KUMRAL, ZARİFE NİGAR
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ÖZDEMİR KUMRAL
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ZARİFE NİGAR
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Publication Metadata only Obestatin improves ischemia/reperfusion-induced renal injury in rats via its antioxidant and anti-apoptotic effects: Role of the nitric oxide(ELSEVIER SCIENCE INC, 2014) YEGEN, BERRAK; Koc, Mehmet; Kumral, Zarife Nigar Ozdemir; Ozkan, Naziye; Memi, Gulsun; Kacar, Omer; Bilsel, Serpil; Cetinel, Sule; Yegen, Berrak C.Obestatin was shown to have anti-inflammatory effects in several inflammatory models. To elucidate the potential renoprotective effects of obestatin, renal I/R injury was induced in male Sprague Dawley rats by placing a clamp across left renal artery for 60 min following a right nephrectomy. Clamp was released and the rats were injected with either saline or obestatin (10, 30, 100 mu g/kg). In some experiments, obestatin (10 mu g/kg) was administered with L-NAME (10 mg/kg) or L-Nil (0.36 mg/kg). Following a 24-h reperfusion, the rats were decapitated to measure serum creatinine and nitrite/nitrate levels, renal malondialdehyde (MDA), glutathione (GSH) levels and myeloperoxidase (MPO) activity and to assess cortical necrosis and apoptosis scores. Obestatin treatment reduced I/R-induced increase in creatinine levels, renal MPO activity and renal MDA levels, while renal GSH levels were significantly increased by obestatin. Histological analysis revealed that severe I/R injury and high apoptosis score in the kidney samples of saline-treated rats were significantly reduced and the cortical/medullary injury was ameliorated by obestatin. Expression of eNOS, which was increased by I/R injury, was further increased by obestatin, while serum NO levels were significantly decreased. iNOS inhibitor L-Nil reduced oxidative renal damage and improved the functional and histopathological parameters. I/R-induced elevation in eNOS expression, which was further increased by obestatin, was depressed by L-NAME and L-Nil treatments. The present data demonstrate that obestatin ameliorates renal I/R-injury by its possible anti-oxidative, anti-inflammatory and anti-apoptotic properties, which appear to involve the suppression of neutrophil accumulation and modulation of NO metabolism. (C) 2014 Elsevier Inc. All rights reserved.Publication Metadata only Serum Leptin, Obestatin, and Ghrelin Levels and Gastric Emptying Rates of Liquid and Solid Meals in Non-obese Rats with Roux-en-Y Bypass Surgery or Prosthesis Placement: Implications for the Role of Vagal Afferents(SPRINGER, 2017) YEGEN, BERRAK; Yavuz, Yunus; Kumral, Zarife Nigar Ozdemir; Memi, Gulsun; Cevik, Ozge Dagdeviren; Yegen, Cumhur; Yegen, Berrak C.Background The present study aimed to investigate the effects of Roux-en-Y gastric bypass (RYGB) and prosthesis placement on gastric emptying rate in conjunction with serum ghrelin-obestatin-leptin responses in non-obese rats with intact or denervated afferent innervation. Methods Under anesthesia, male Sprague-Dawley rats underwent either sham operation, RYGB, prosthesis, and/or Gregory cannula placement. Three weeks later, liquid or solid gastric emptying tests were performed and serum ghrelin, leptin and obestatin levels were measured. Results Both prosthesis placement and RYGB surgery delayed non-nutrient liquid emptying; while solid nutrient emptying was delayed only by RYGB. Nutrient-dependent (acid, hyperosmolal and peptone) delay in liquid emptying was abolished in rats with prosthesis. By vagal afferent denervation, delayed liquid emptying was abolished, while solid emptying was further delayed in rats with prosthesis. Ghrelin and obestatin levels were depressed in prosthesis-placed rats, but RYGB surgery had no impact on both levels. Leptin level was elevated in solid-food-given rats with prosthesis, but not changed in RYGB group, while it was reduced following liquid meal. All the changes observed in ghrelin, obestatin, or leptin levels in response to meal ingestion were reversed with vagal afferent denervation. Conclusions Both RYGB and prosthesis placement had delaying effects on gastric emptying rate of non-obese rats. Our results indicate that the short-term changes in gastric motility and hormone responses induced by volume reduction are reversed by afferent denervation, suggesting that sparing the vagal innervation could be essential for reaching optimum motility and hormone changes expected after bariatric surgery.Publication Metadata only Functional and structural changes of the urinary bladder following spinal cord injury; treatment with alpha lipoic acid(WILEY, 2017) VELİOĞLU ÖĞÜNÇ, AYLİZ; Ekiz, Arif; Ozdemir-Kumral, Zarife Nigar; Ersahin, Mehmet; Tugtepe, Halil; Ogunc, Ayliz Velioglu; Akakin, Dilek; Kiran, Demir; Ozsavci, Derya; Biber, Necat; Hakan, Tayfun; Yegen, Berrak C.; Sener, Goksel; Toklu, Hale Z.BACKGROUND & AIMAlpha lipoic acid (LA) was shown to exert neuroprotection in trauma-induced spinal cord injury (SCI), which is frequently associated with urinary bladder complaints in patients with SCI. Accordingly, the protective effects of LA on biochemical and histological changes in bladder as well as functional studies were assessed. METHODSWistar albino rats were divided as control, SCI, and LA (50mg/kg/day, ip) treated SCI groups (SCI+LA). The standard weight-drop (100g/cm force at T10) method was used to induce a moderately severe SCI. One week after the injury, neurological examination was performed and the rats were decapitated. Bladder samples were taken for histological examination, functional (isolated tissue bath) studies, and for the measurement of biochemical parameters (malondialdehyde, MDA; gluthathione, GSH; nerve growth factor, NGF; caspase-3, luminol and lucigenin chemiluminescences). RESULTSSCI caused a significant (P<0.001) increase in the detrusor muscle thickness. It increased the contractility responses to carbachol and relaxation responses to papaverine (P<0.05-0.001). There were also significant alterations in MDA, caspase-3, luminol, and lucigenin chemiluminescences with concomitant decreases in NGF and GSH (P<0.05). LA treatment reversed histological and functional (contraction and relaxation responses) changes induced by SCI (P<0.05-0.001), but no significant recovery was observed in the impaired neurological functions. CONCLUSIONThese results indicate that LA have a beneficial effect in improving the bladder tonus via its antioxidant and anti-inflammatory actions following SCI.Publication Metadata only Protective Effect of Nicotine on Sepsis-Induced Oxidative Multiorgan Damage: Role of Neutrophils(OXFORD UNIV PRESS, 2017) YEGEN, BERRAK; Ozdemir-Kumral, Zarife N.; Ozbeyli, Dilek; Ozdemir, Ahmet F.; Karaaslan, Bugra M.; Kaytaz, Kubra; Kara, Mustafa F.; Tok, Olgu E.; Ercan, Feriha; Yegen, Berrak C.Despite its adverse health consequences, tobacco smoking is associated with lower incidence of several neurodegenerative and inflammatory diseases. The present study is aimed to show the effects of nicotine, major tobacco constituent, on five organs targeted by sepsis. Male Wistar albino rats received tap water with (5mg/kg) or without nicotine for 14 days. Under ketamine anesthesia, sepsis (n = 50) was induced by ligation and puncture of the cecum, while sham group (n = 8) had only laparotomy. In other rats, nicotine drink was withdrawn for 5 days before sepsis induction, while in acute nicotine group, rats were injected with nicotine (30mg/kg, i.p.) before sepsis, but had no oral intake. Rats were decapitated 24 hours after surgery to obtain lung, liver, ileum, heart, and kidney tissues to determine malondialdehyde (MDA) and glutathione (GSH) levels and myeloperoxidase (MPO) activities. Data were analyzed by one-way analysis of variance and Tukey multiple comparison tests or Student's t test. Chronic nicotine administration or its withdrawal reduced lipid peroxidation and MPO activity and prevented GSH depletion with some varying results in different target tissues. Nicotine injection prior to sepsis depressed MPO activity in all tissues and reduced MDA levels except for the lung, while GSH levels were elevated only in the hepatic and ileal tissues. Histologically observed injury was ameliorated by all nicotine treatments at varying degrees. The findings of the present study indicate that long-term nicotine administration reduces sepsis-induced oxidative damage in several tissues, which appears to involve inhibition of neutrophil activity in the inflamed tissues. Nicotine administration or its withdrawal reduced lipid peroxidation and neutrophil content and prevented GSH depletion with some varying results in different target tissues. A single injection prior to sepsis induction depressed MPO activity in all the tissues and reduced all tissue MDA levels except for the lung. When nicotine was withdrawn for 5 days, its inhibitory effect on MPO activity was still present in all the tissues except for the liver. Microscopically an improved inflammatory response was observed in all the tissues of rats that have received different nicotine pretreatment regimens.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 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 Estrogen Alleviates Acetic Acid-Induced Gastric or Colonic Damage via Both ER alpha- and ER beta-Mediated and Direct Antioxidant Mechanisms in Rats(SPRINGER/PLENUM PUBLISHERS, 2014) YEGEN, BERRAK; Kumral, Zarife Nigar Ozdemir; Memi, Gulsun; Ercan, Feriha; Yegen, Berrak C.In order to demonstrate the possible protective effects of estrogen receptor (ER)-alpha and ER beta receptor subtypes in the pathogenesis of colonic and gastric oxidant damage, experimental ulcer and colitis were induced by acetic acid, and the animals were randomly divided as colitis, ulcer, and their corresponding non-ulcer and non-colitis control groups. Each group of rats was treated intramuscularly with the vehicle, selective ER alpha agonist propylpyrazole-triol (1 mg/kg), ER beta agonist diarylpropionitrile (1 mg/kg), non-selective ER agonist 17 beta estradiol (E2; 1 mg/kg), or E2 plus non-selective ER antagonist ICI-182780 (1 mg/kg). The results revealed that induction of ulcer or colitis resulted in systemic inflammation as assessed by increased levels of plasma TNF-alpha and IL-6 levels. In both tissues, the presence of oxidant damage was verified by histological analysis and elevated myleoperoxidase activity. In the colitis and ulcer groups, both ER agonists and the non-selective E2 reversed the oxidative damage in a similar manner. These findings indicate that estrogen acts via both ER alpha- and ER beta-mediated and direct antioxidant mechanisms, where both ER subtypes play equal and efficient roles in the anti-inflammatory action of estrogen, in limiting the migration of neutrophils to the inflamed tissue, reducing the release and activation of cytokines and thereby alleviating tissue damage.Publication Metadata only Nesfatin-1 Ameliorates Sepsis-Induced Remote Organ Injury: The Role of Oxidant-Antioxidant Status and Neutrophils(MARMARA UNIV, INST HEALTH SCIENCES, 2018) YEGEN, BERRAK; Ozdemir-Kumral, Zarife Nigar; Cumhur, Ahmet; Oluk, Ali Ihsan; Hoscan, Aykut; Onem, Idris; Contuk, Gazi; Ercan, Feriha; Yegen, Berrak C.Purpose: Protective effects of nesfatin-1 was studied in sepsis-induced injury of remote organs. Methods: Male rats were randomly divided as control and sepsis (cecal ligation-perforation) groups, treated with either saline or nesfatin-1 (10 mu g/kg). At 16 h following surgery, samples of brain, kidney, liver and lung tissues were removed and myeloperoxidase (MPO) activity, glutathione (GSH), catalase (CAT), superoxide dismutase (SOD) and malondialdehyde (MDA) levels were measured in these tissues. Results: In saline-treated septic rats, elevated MDA and MPO activities were accompanied with depleted CAT, SOD and GSH levels in the brain, kidney, liver and lung tissues, implicating extensive oxidative damage in all remote organs. Nesfatin-1 reduced MDA levels (brain, lung) and MPO activities (brain, kidney), and preserved antioxidant GSH (brain, lung), CAT (brain) and SOD (kidney) levels. Severe hepatocyte degeneration, neuronal damage, glomerulotubular degeneration and alveolar disturbance in saline-treated septic rats were replaced with regular tissue morphologies in nesfatin-1-treated rats. Conclusion: Nesfatin-1 alleviates oxidative damage by enhancing endogenous antioxidant systems and inhibiting recruitment of neutrophils, suggesting that nesfatin-1 may be have a potential therapeutic impact on the treatment of septic shock to reduce subsequent remote organ failure.Publication Metadata only Phoenixin-14 Sepsise Bağlı Gelişen Kardiyopulmoner Hasarı Hafifletir: Vagal Tonusun Rolü(2021-10-10) ÖZDEMİR KUMRAL, ZARİFE NİGAR; UPRAK, TEVFİK KIVILCIM; YEGEN, BERRAK; ÖZDEMİR KUMRAL Z. N., ŞEN L. S., Çantalı Öztürk Ç., UPRAK T. K., YEGEN B.AMAÇ: Sepsis, sistemik inflamasyon ve yaşamsal organların disfonksiyonu ile tanımlanan yıkıcı bir hastalıktır. Phoenixin’in (PNX-14) çoğunlukla hipotalamusta ve kalpte eksprese olduğu ve iskemiyi takiben kardiyoproteksiyon sağladığı gösterilmiştir. Çalışmanın amacı, PNX-14'ün sepsis kaynaklı kardiyopulmoner hasar üzerinde yararlı etkisinin olup olmadığını değerlendirmek ve vagal liflerin bu etkiye katkısını açıklamaktır. YÖNTEMLER: Ketamin anestezisi altında, erkek SpragueDawley sıçanlara (310-390 g) taklit cerrahi (n=8) veya sepsisi indüklemek için çekal ligasyon ve ponksiyon (n=23) yapıldı. Sepsis yapılmadan önce, serum fizyolojik veya PNX-14 (50 µg/kg/gün) son 36 saat içinde tekrarlayan 3 doz şeklinde intraperitoneal olarak uygulandı. PNX-14 tedavisi alan sıçanların yarısında ek olarak vagal stimülasyon (VS) yapılırken diğerlerine VS yapılmadı. VS amacıyla sıçanlara, sepsisten 7 gün önce başlayarak, diazepam (5mg/kg) anestezisi altında aurikula konkalarındaki elektrotlar aracılığıyla düşük seviyeli transkutanöz VS (20 Hz, 0,2ms, 2mA, 30 dk/gün) uygulandı. Sepsisin 16. saatinde serum TNF-α ve IL-6 düzeylerini ölçmek için kardiyak ponksiyonla kan alındı, histolojik değerlendirme ve miyeloperoksidaz aktivitesi, glutatyon, katalaz, süperoksit dismutaz (SOD), malondialdehit seviyelerinin belirlenmesi için kalp ve akciğer örnekleri alındı. Veriler Student t-testi ve tek-yönlü ANOVA kullanılarak analiz edildi. BULGULAR: Sepsis, her iki dokuda hipotermiye, serum TNF-α ve IL-6 seviyelerinde artışa, her iki dokuda miyeloperoksidaz aktivitesinde ve histolojik hasar skorlarında artışa neden olurken, katalaz ve glutatyon seviyelerinde azalmaya neden oldu (p<0,05-0,001). Ayrıca, septik sıçanların kalp dokularında malondialdehit ve SOD seviyelerinin de yükseldiği gözlendi (p<0,05). PNX-14 hipotermiyi, her iki dokunun miyeloperoksidaz aktivitesini ve hasar skorlarını azaltırken, kalp dokusunda malondialdehit seviyesini düşürdü. Ayrıca, PNX ile kardiyak glutatyon, katalaz düzeyleri ve akciğerde SOD seviyeleri artmış bulundu (p<0,05-0,001). PNX tedavisi ile her iki dokunun histolojik skorlarında ve kalp dokusu malondialdehit seviyesindeki gözlenen azalmalar ile kalp dokusunun glutatyon ve katalaz düzeylerinde ve akciğerin SOD seviyelerindeki artışlar VS ile tersine çevrildi. SONUÇ: PNX-14, sepsise bağlı kalp ve akciğerde gözlenen oksidatif hasarı iyileştirmektedir ve bunu kısmen vagal tonus üzerindeki inhibitör etkiyle gerçekleştirmektedir.Publication Metadata only Alpha-7 nicotinic receptor agonist GTS-21 ameliorates contrast-induced nephropathy in rats(2019-10-05) AKÇAY, SEÇKİN; ÖZDEMİR KUMRAL, ZARİFE NİGAR; PEKER EYÜBOĞLU, İREM; YEGEN, BERRAK; AKÇAY S., ÖZDEMİR KUMRAL Z. N., çilingir kaya ö. T., PEKER EYÜBOĞLU İ., AKKİPRİK M., YEGEN B.