Person: YÜKSEL, MERAL
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YÜKSEL
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Publication Metadata only Apocynin attenuates testicular ischemia-reperfusion injury in rats(W B SAUNDERS CO-ELSEVIER INC, 2015) ŞİMŞEK, FERRUH; Sener, T. Emre; Yuksel, Meral; Ozyilmaz-Yay, Nagehan; Ercan, Feriha; Akbal, Cem; Simsek, Ferruh; Sener, GokselObjective: This study was designed to examine the possible protective effect of apocynin, a NADPH oxidase inhibitor, against torsion/detorsion (T/D) induced ischemia/reperfusion (I/R) injury in testis. Methods: Male Wistar albino rats were divided into sham-operated control, and either vehicle, apocynin 20 mg/kg-or apocynin 50 mg/kg-treated T/D groups. In order to induce I/R injury, left testis was rotated 720 degrees clockwise for 4 hours (torsion) and then allowed reperfusion (detorsion) for 4 hours. Left orchiectomy was done for the measurement of tissue malondialdehyde (MDA), glutathione (GSH) levels, myeloperoxidase (MPO) activity, and luminol, lucigenin, nitric oxide (NO) and peroxynitrite chemiluminescences (CL). Testicular morphology was examined by light microscopy. Results: I/R caused significant increases in tissue luminol, lucigenin, nitric oxide and peroxynitrite CL demonstrating increased reactive oxygen and nitrogen metabolites. As a result of increased oxidative stress tissue MPO activity, MDA levels were increased and antioxidant GSH was decreased. On the other hand, apocynin treatment reversed all these biochemical indices, as well as histopathological alterations that were induced by I/R. According to data, although lower dose of apocynin tended to reverse the biochemical parameters, high dose of apocynin provides better protection since values were closer to the control levels. Conclusion: Findings of the present study suggest that NADPH oxidase inhibitor apocynin by inhibiting free radical generation and increasing antioxidant defense exerts protective effects on testicular tissues against I/R. The protection with apocynin was more pronounced with high dose. (C) 2015 Elsevier Inc. All rights reserved.Publication Metadata only Erdosteine treatment attenuates oxidative stress and fibrosis in experimental biliary obstruction(SPRINGER, 2007) ERCAN, FERİHA; Sener, Goeksel; Sehirli, A. Ozer; Toklu, Hale Z.; Yuksel, Meral; Ercan, Feriha; Gedik, NursalOxidative stress, in particular lipid peroxidation, induces collagen synthesis and causes fibrosis. The aim of this study was to assess the antioxidant and antifibrotic effects of erdosteine on liver fibrosis induced by biliary obstruction in rats. Liver fibrosis was induced in Wistar albino rats by bile duct ligation (BDL). Erdosteine (10 mg/kg, orally) or saline was administered for 28 days. Serum aspartate aminotransferase (AST), alanine aminotransferase (ALT) and lactate dehydrogenase (LDH) levels were determined to assess liver functions and tissue damage, respectively. Pro-inflammatory cytokines, TNF-alpha, IL-1 beta and IL-6 and antioxidant capacity (AOC) were assayed in plasma samples. Liver tissues were taken for determination of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity and collagen content. Production of reactive oxidants was monitored by chemiluminescence assay. Serum AST, ALT, LDH, and plasma cytokines were elevated in the BDL group as compared to controls and were significantly decreased by erdosteine treatment. Hepatic GSH level and plasma AOC, depressed by BDL, were elevated back to control level with erdosteine treatment. Furthermore, hepatic luminol and lucigenin chemiluminescence (CL), MDA level, MPO activity and collagen content in BDL group increased dramatically compared to control and reduced by erdosteine treatment. Since erdosteine administration alleviated the BDL-induced oxidative injury of the liver and improved the hepatic functions, it seems likely that erdosteine with its antioxidant and antifibrotic properties, may be of potential therapeutic value in protecting the liver fibrosis and oxidative injury due to biliary obstruction.Publication Metadata only Better lung protection following death due to rapid exsanguination in rats(BAYCINAR MEDICAL PUBL-BAYCINAR TIBBI YAYINCILIK, 2012) LAÇİN, BERNA; Bostanci, Korkut; Lacin, Berna Karakoyun; Yuksel, Meral; Ercan, Feriha; Yuksel, Mustafa; Batirel, Hasan FevziBackground: This study aims to investigate the effects of death due to rapid exsanguination on the viability of lung tissue. Methods: Fourty-six Sprague-Dawley male rats with a weight range of 310-370 g were included in the study. Rats were divided into six groups: (i) ischemic alone (I group; n=8); (ii) passive exsanguination group of whose major abdominal veins were cut following death (PE group; n=8) (iii) group of whose major abdominal veins were cut and sacrified with rapid exsanguination (RE group; n=8); (iv) lung perfusion group with saline (SP group; n=8); (v) lung perfusion group with Perfadex (PP group; n=8) and (vi) control group (C group; n=6). Rats in all experiement groups except rapid exsanguination ones and all in the control group were euthanized with intrahepatic pentobarbital. Lungs were removed following euthanasia in the controls. In all study groups, lungs were ventilated in the cadavers at room temperature for 120 minutes and kept in warm ischemia. Results: Myeloperoxidase (MPO) activity, luminol chemiluminescence (CL) values and non-viable cell rate were higher in the ischemia group. The PE group had increased MPO activity, lucigenin CL values and nonviable cell rate, whereas the RE group had reduced MPO activity and luminol CL values, compared to ischemia group. MPO activity, lucigenin CL levels and non-viable cell rate were lower in the RE group, compared to PE. The PP had lower MPO activity and luminol CL values, compared to SP or ischemia group, whereas non-viable cell rate increased. Conclusion: Death following rapid exsanguination results in better preservation of lung viability and minimal oxidative injury. This may be explained by rapid loss of platelets and inflammatory cells in the tissue and shift of extravascular fluid to intravascular compartment.Publication Metadata only THERAPEUTIC POTENTIAL OF MYRTUS COMMUNIS SUBSP COMMUNIS EXTRACT AGAINST ACETIC ACID-INDUCED COLONIC INFLAMMATION IN RATS(WILEY, 2017) ŞEN, ALİ; Sen, Ali; Yuksel, Meral; Bulut, Gizem; Bitis, Leyla; Ercan, Feriha; Ozyilmaz-Yay, Nagehan; Akbulut, Ozben; Cobanoglu, Hamit; Ozkan, Sevil; Sener, GokselThe aim of this study was to evaluate the effect of ethanol extract from leaves of Myrtus communis subsp. communis (MC) on acetic acid (AA)-induced ulcerative colitis in rats. On the fourth day of colitis induction, all rats were decapitated. Colitis was assessed by macroscopic and microscopic scores and by measuring malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity, luminol, lucigenin, nitric oxid and peroxynitrite chemiluminescence (CL). Colitis caused significant increases in the colonic MDA levels, MPO activity, CL values, macroscopic and microscopic damage scores along with significant decrease in tissue GSH level. However, treatment with MC extract reversed all these biochemical indices, as well as histopathological alterations induced by AA with the protective effects being similar to that of sulphasalazine treatment. The study showed that MC extract could alleviate colitis in rats and can be considered an alternative therapeutic approach for management of inflammatory bowel diseases (IBD).Publication Metadata only Protective effects of Ginkgo biloba against acetaminophen-induced toxicity in mice(SPRINGER, 2006) ERCAN, FERİHA; Sener, G; Omurtag, GZ; Sehirli, O; Tozan, A; Yuksel, M; Ercan, F; Gedik, NBackground: The analgesic acetaminophen (AAP) causes a potentially fatal, hepatic centrilobular necrosis when taken in overdose. It was reported that these toxic effects of AAP are due to oxidative reactions that take place during its metabolism. Objective: In this study, we aimed to investigate the possible beneficial effect of Ginkgo biloba (EGb), an antioxidant agent, against AAP toxicity in mice. Methods: Balb/c mice were injected i.p. with: (1) vehicle, control (C) group; (2) a single dose of 50 mg/kg Ginkgo biloba extract, EGb group; (3) a single dose of 900 mg/kg i.p. acetaminophen, AAP group, and (4) EGb, in a dose of 50 mg/kg after AAP injection, AAP + EGb group. Serum ALT, AST, and tumor necrosis factor-alpha (TNF-alpha) levels in blood and glutathione (GSH), malondialdehyde (MDA) levels, myeloperoxidase (MPO) activity, and collagen contents in liver tissues were measured. Formation of reactive oxygen species in hepatic tissue samples was monitored by using chemiluminescence (CL) technique with luminol and lusigenin probe. Tissues were also examined microscopically. Results: ALT, AST levels, and TNF-alpha were increased significantly (p < 0.001) after AAP treatment, and reduced with EGb. Acetaminophen caused a significant (p < 0.05-0.001) decrease in GSH levels while MDA levels and MPO activity were increased (p < 0.001) in liver tissues. These changes were reversed by EGb treatment. Furthermore, luminol and lusigenin CL levels in the AAP group increased dramatically compared to control and reduced by EGb treatment (p < 0.01). Conclusion: Our results implicate that AAP causes oxidative damage in hepatic tissues and Ginkgo biloba extract, by its antioxidant effects protects the tissues. Therefore, its therapeutic role as a tissue injury-limiting agent must be further elucidated in drug-induced oxidative damage.Publication Metadata only The role of cholinergic anti-inflammatory pathway in acetic acid-induced colonic inflammation in the rat(ELSEVIER IRELAND LTD, 2013) VELİOĞLU ÖĞÜNÇ, AYLİZ; Kolgazi, Meltem; Uslu, Unal; Yuksel, Meral; Velioglu-Ogunc, Ayliz; Ercan, Feriha; Alican, InciThe cholinergic anti-inflammatory pathway'' provides neurological modulation of cytokine synthesis to limit the magnitude of the immune response. This study aimed to evaluate the impact of the cholinergic anti-inflammatory pathway on the extent of tissue integrity, oxidant-antioxidant status and neutrophil infiltration to the inflamed organ in a rat model of acetic acid-induced colitis. Colitis was induced by intrarectal administration of 5% acetic acid (1 ml) to Sprague-Dawley rats (200-250 g; n = 7-8 per group). Control group received an equal volume of saline intrarectally. The rats were treated with either nicotine (1 mg/kg/day) or huperzine A (0.1 mg/kg/day) intraperitoneally for 3 days. After decapitation, the distal colon was scored macroscopically and microscopically. Tissue samples were used for the measurement of malondialdehyde (MDA) and glutathione (GSH) levels, and myeloperoxidase (MPO) activity. Formation of reactive oxygen species was monitored by using chemiluminescence (CL). Nuclear factor (NF)-kappa B expression was evaluated in colonic samples via immunohistochemical analysis. Trunk blood was collected for the assessment of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1 beta, IL-10, resistin and visfatin levels. Both nicotine and huperzine A reduced the extent of colonic lesions, increased colonic MDA level, high MPO activity and NF-kappa B expression in the colitis group. Elevation of serum IL-1 beta level due to colitis was also attenuated by both treatments. Additionally, huperzine A was effective to reverse colitis-induced high lucigenin-enhanced CL values and serum TNF-alpha levels. Colitis group revealed decreased serum visfatin levels compared to control group which was completely reversed by nicotine. In conclusion, modulation of the cholinergic system either by nicotine or ACh esterase inhibition improved acetic acid-induced colonic inflammation as confirmed by macroscopic and microscopic examination and biochemical assays. (C) 2013 Elsevier Ireland Ltd. All rights reserved.Publication Open Access Burn-induced distant organ ınjury in rats and the effect of minocycline(2017-10-15) ERCAN, FERİHA; Bahadir, Elif; Sancar, Murat; Tarhan, Gazi Giray; Koçak, Emre; Budancamanak, Zeynep; Karaaslan, Seda; Kervancioğlu Demi̇Rci̇, Elif; Yüksel, Meral; Ercan, Feriha; Ali̇Can, İnciPublication Metadata only Effect of phosphodiesterase-5 inhibition on joint and muscle damage in rats with adjuvant arthritis(TUBITAK SCIENTIFIC & TECHNICAL RESEARCH COUNCIL TURKEY, 2018) ERCAN, FERİHA; Bahadir, Faize Elif; Koroglu, Mustafa Kutay; Yuksel, Meral; Ercan, Feriha; Alican, Y. InciBackground/aim: This study was designed to examine the effect of tadalafil, a phosphodiesterase (PDE) 5 inhibitor, on the severity of joint and muscle damage in rats with adjuvant-induced arthritis (AA). Materials and methods: AA was induced by intradermal inoculation into right hind paw of male Sprague Dawley rats (300-450 g) with complete Freund's adjuvant (CFA; 0.1 mL). AA rats were treated with either tadalafil (10 mg/kg; per oral) alone or along with the soluble guanylyl cyclase inhibitor 1H-[1,2,4] oxadiazolo[4,3-a] quinoxalin-1-one (ODQ; 10 mg/kg; intraperitoneally). After decapitation on day 16, trunk blood was collected for total oxidant status (TOS) and total antioxidant capacity (TAC) assays. The left metatarsophalangeal joint and gastrocnemius muscle were excised for microscopic examination. Muscle samples were also evaluated in terms of malondialdehyde (MDA), glutathione, and chemiluminescence (CL) levels. Results: In tadalafil-treated AA rats, metatarsophalangeal joints revealed regular morphology of the cartilage with slight destruction and less inflammatory cell infiltration and vascularization in comparison to the controls (microscopic score: 1.17 +/- 0.31 vs. 4.17 +/- 0.79; P < 0.01). AA rats presented increased gastrocnemius muscle MDA, glutathione, and CL levels compared to the controls (P < 0.01, for MDA; P < 0.05, for glutathione; P < 0.05 for CL). Tadalafil attenuated the increase in CL levels (P < 0.01, for luminol and P < 0.001, for lucigenin). Serum TOS showed significant reductions by tadalafil. Conclusion: The long-acting PDE5 inhibitor tadalafil provides partial protection in a rat model of CFA-induced arthritis possibly via suppression of oxidant generation.Publication Metadata only Alpha-Lipoic Acid Improves Acetic Acid-Induced Gastric Ulcer Healing in Rats(SPRINGER/PLENUM PUBLISHERS, 2009) YEGEN, BERRAK; Karakoyun, Berna; Yuksel, Meral; Ercan, Feriha; Erzik, Can; Yegen, Berrak C.To evaluate the role of ALA treatment on the healing of acetic acid-induced gastric ulcer, rats were given ALA (35 mg/kg/day) or saline for 3 days before the induction of ulcer and the treatment was continued twice daily for 2 days (early) or 10 days (late) until they were decapitated. Gastric ulcer index, microscopic score, elevated DNA fragmentation and chemiluminescence levels of the saline-treated ulcer groups were all reduced by ALA treatment. Likewise, ALA treatment inhibited chemiluminescence levels in both early and late ulcer groups. Marked reduction in glutathione levels of the saline-treated early ulcer group was reversed by ALA treatment, while ALA treatment was effective in depressing gastric myeloperoxidase activity in the late ulcer group. In conclusion, ALA treatment shows protective role in the healing of acetic acid-induced gastric injury in rats via the suppression of neutrophil accumulation, preservation of endogenous glutathione, inhibition of reactive oxidant generation and apoptosis.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.