Person: ERCAN, FERİHA
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ERCAN
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FERİHA
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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 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 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 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 Simvastatin attenuates cisplatin-induced kidney and liver damage in rats(ELSEVIER IRELAND LTD, 2007) ERCAN, FERİHA; Iseri, Sevgin; Ercan, Feriha; Gedik, Nursal; Yuksel, Meral; Alican, InciStatins have anti-inflammatory effects that are not directly related to their cholesterol-lowering activity. This study aimed to investigate the effect of simvastatin on the extent of tissue damage in cisplatin-induced nephrotoxicity and hepatotoxicity. The rats received a single intravenous injection of 2.5 mg kg(-1) cisplatin. Other groups received either simvastatin (1 mg kg(-1)) or the vehicle (ethanol: saline) intraperitoneally for 10 days beginning 5 days prior to cisplatin injection. All animals were decapitated 5 days after cisplatin administration. Trunk blood was collected and analyzed for blood urea nitrogen (BUN), creatinine, alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), albumin, and total bilirubin levels. The urine samples were used for the calculation of creatinine clearance levels. The kidney and liver samples were stored for the measurement of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity and collagen content or were processed for histopathological examinations. Formation of reactive oxygen species in tissue samples was monitored by using chemiluminescence method. Simvastation reduced the extent of both kidney and liver damage and preserved both kidney and liver functions (p < 0.01-0.001). Increase in liver MDA level with a concomitant reduction in GSH in the cisplatin group was attenuated by simvastatin treatment (p < 0.05-0.01). Increase in tissue collagen content and chemiluminescence levels in the kidney and liver samples of the cisplatin group was also reversed by simvastatin (p < 0.001). In conclusion, simvastatin is beneficial in cisplatin-induced kidney and liver dysfunction and organ damage in rats via prevention of lipid peroxidation and tissue fibrosis, preservation of antioxidant glutathione, and suppression of neutrophil infiltration. (c) 2006 Elsevier Ireland Ltd. All rights reserved.Publication Metadata only Treatment with estrogen receptor agonist ER beta improves torsion-induced oxidative testis injury in rats(PERGAMON-ELSEVIER SCIENCE LTD, 2019) YILDIRIM, ALPER; Tamer, Sevil Arabaci; Yildirim, Alper; Arabaci, Sule; Ciftci, Selin; Akin, Sena; Sari, Elif; Koroglu, M. Kutay; Ercan, Feriha; Yuksel, Meral; Cevik, Ozge; Yegen, Berrak C.Aims: The purpose of the present study was to investigate the potential antioxidant, anti-apoptotic and sperm function-preserving effects of estrogen, estrogen receptor (ER) a and ER beta agonists in a rat model of testis torsion-detorsion (T/D). Main methods: Under anesthesia, 6-8-week-old male Sprague-Dawley rats underwent sham-operation or testicular torsion by fixing left testis rotated at 720 degrees for 2 h. After detorsion, rats were treated with ER alpha agonist (1 mg/kg/day, subcutaneously, sc) or ER beta agonist (1 mg/kg/day, sc) or estradiol (E-2, 1 mg/kg/day, in drinking water) or vehicle on the following two days. On the third day, testicular blood-flow was recorded and then left testes were extracted for molecular and histochemical analysis. Key findings: The findings showed that reduced testicular blood-flow following torsion was partially restored on the 3rd day of detorsion, while treatments with either of the ER agonists or E-2 returned blood flow fully back to the control levels. When the testis-torsioned rats were given ER beta agonist during the detorsion period, tubular injury was lessened, sperm count and motility were increased, while the production of reactive oxygen meta-bolites and apoptosis in the testis tissues were totally suppressed. Although a down-regulated expression of androgen receptor (AR) along with a reduction in serum testosterone level was observed in the vehicle-treated T/D group, all three treatments up-regulated the expressions of AR and its mRNA, while ER alpha agonist and E-2 suppressed the testosterone level. Significance: ER beta receptor activation during the post-ischemic period may be beneficial in protection against torsion-related oxidant testicular injury and infertility.