Person: ÖZDEMİR KUMRAL, ZARİFE NİGAR
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ÖZDEMİR KUMRAL
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ZARİFE NİGAR
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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 In other rats, nicotine drink was withdrawn for 5 days before sepsis induction, while in acute nicotine group, rats were injected with nicotine (30mg/kg, i.p.) before sepsis, but had no oral intake.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 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 Potential Effect of 1,25 Dihydroxyvitamin D-3 on Thioacetamide-Induced Hepatotoxicity in Rats(ACADEMIC PRESS INC ELSEVIER SCIENCE, 2019) YÜKSEL, MERAL; Ozdemir-Kumral, Zarife N.; Erkek, Burak E.; Karakus, Buse; Almaci, Meslina; Fathi, Reza; Yuksel, Meral; Cumbul, Alev; Alican, InciBackground: 1,25 Dihydroxyvitamin D-3 (1,25(OH)(2)D-3) modulates inflammation and immune responses. Deficiency of 1,25(OH)(2)D-3 was found to be associated with the risk of cancer, cardiovascular disease, osteoarthritis, infections, and autoimmune diseases. This study evaluated the effect of 1,25 dihydroxyvitamin D-3 1,25(OH)(2)D-3 on thioacetamide (TAA)-induced acute liver injury in rats. Materials and methods: Rats were treated with either saline or 1,25(OH)(2)D-3 (0.30 mg/kg; orogastrically) for 15 d. Starting from day 13, TAA (200 mg/kg; intraperitoneally) was given for 3 d. On day 15, all rats were euthanized. Liver and blood samples were collected. Results: TAA caused severe damage, increased lipid peroxidation with reductions in endogenous antioxidants, increased apoptosis, increased production of reactive oxygen species, and elevated inducible nitric oxide synthase (iNOS), and nuclear factor kappa B (NF-kappa B) expression in liver. Extent of damage was decreased by 1,25(OH)(2)D-3 (P < 0.01). 1,25(OH)(2)D-3 attenuated the increase in malondialdehyde (P < 0.01), increase in myeloper-oxidase (P < 0.01), increase in chemiluminescence levels (P < 0.05) and apoptotic activity (P < 0.001). Elevated liver iNOS and NF-kappa B expression in TAA group was also reduced by 1,25(OH)(2)D-3 (P < 0.001, for iNOS; P < 0.001, for NF-kappa B). TAA group revealed high serum aspartate transaminase and alanine transaminase (ALT) activities (P < 0.01, for aspartate transaminase; P = 0.08, for ALT) and reduced albumin levels (P < 0.01) compared with control. 1,25(OH)(2)D-3 had no statistically significant effect on these parameters. Conclusions: 1,25(OH)(2)D-3 provides protection against hepatic injury in a rat model of TAA-induced hepatotoxicity via suppression of inflammatory reaction, oxidative stress, and apoptosis. (C) 2019 Elsevier Inc. All rights reserved.Publication Open Access The gastroprotective effect of obestatin on indomethacin-induced acute ulcer is mediated by a vagovagal mechanism(AKADEMIAI KIADO ZRT, 2020-06) YEGEN, BERRAK; Sen, Leyla Semiha; Kumral, Zarife Nigar Ozdemir; Memi, Gulsun; Ercan, Feriha; Yegen, Berrak C.; Yegen, CumhurIn order to investigate the role of the vagus nerve in the possible gastroprotective effect of obestatin on the indomethacin-induced acute oxidative gastric injury, Sprague-Dawley rats of both sexes were injected subcutaneously with indomethacin (25 mg/kg, 5% NaHCO3) followed by obestatin (10, 30 or 100 mu g/kg). In other sets of rats, surgical vagotomy (Vx) or selective degeneration of vagal afferent fibers by perivagal capsaicin was performed before the injections of indomethacin or indomethacin + obestatin (30 mu g/kg). Gastric serosal blood flow was measured, and 4 h after ulcer induction gastric tissue samples were taken for histological and biochemical assays. Obestatin reduced the severity of indomethacin-induced acute ulcer via the reversal of reactive hyperemia, by inhibiting ulcer-induced neutrophil infiltration and lipid peroxidation along with the replenishment of glutathione (GSH) stores, whereas Vx abolished the inhibitory effect of obestatin on blood flow and lipid peroxidation, and worsened the severity of ulcer. On the other hand, serosal blood flow was even amplified by the selective denervation of the capsaicin-sensitive vagal afferent fibers, but obestatin-induced reduction in ulcer severity was not altered. In conclusion, the gastroprotective effect of obestatin on indomethacin-induced ulcer appears to involve the activation of the vagovagal pathway.