Person: ŞENER, GÖKSEL
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ŞENER
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GÖKSEL
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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 2-mercaptoethane sulfonate (MESNA) protects against biliary obstruction-induced oxidative damage in rats(ELSEVIER IRELAND LTD, 2006) ERCAN, FERİHA; Sener, G; Kabasakal, L; Sehirli, O; Ercan, F; Gedik, NThe aim of this study was to assess the antioxidant and antifibrotic effects of chronic administration of 2-mercaptoethane sulfonate (MESNA) on oxidative liver damage and fibrosis induced by biliary obstruction in rats. Liver fibrosis was induced in male Wistar albino rats by bile duct ligation and scission (BDL). MESNA (150 mg/kg, i.p.) or saline was administered for 28 days. At the end of the experiment, rats were killed by decapitation. Serum aspartate aminotransferase (AST), and alanine aminotransferase (ALT) levels were determined to assess liver function. Tumor necrosis factor-alpha (TNF-alpha) and lactate dehidrogenase (LDH) were also assayed in serum samples. Liver tissues were taken for determination of the free radicals, hepatic malondialdehyde (MDA) levels, an end product of lipid peroxidation; glutathione (GSH) levels, a key antioxidant; myeloperoxidase (MPO) activity, as an indirect index of neutrophil infiltration. Hepatic collagen content, as a fibrosis marker was also determined. Serum AST, ALT, LDH and TNF-alpha levels were elevated in the BDL group as compared to control group, while this increase was significantly decreased by MESNA treatment. BDL caused a significant (p < 0.05-0.001) decrease in GSH levels while MDA levels and MPO activity were increased in the liver tissue. These changes were reversed by MESNA treatment. Collagen contents of the liver tissue was increased by BDL (P < 0.001), and reversed back to the control levels with MESNA. Since MESNA administration alleviated the BDL-induced oxidative injury of the liver and improved the hepatic functions, it seems likely that MESNA with its antioxidant and antifibrotic properties, may be of potential therapeutic value in protecting the liver fibrosis and oxidative injury due to biliary obstruction. (c) 2006 Published by Elsevier Ireland Ltd.Publication Metadata only The protective effects of melatonin against water avoidance stress-induced mast cell degranulation in dermis(ELSEVIER GMBH, 2005) ERCAN, FERİHA; Cikler, E; Ercan, F; Cetinel, S; Contuk, G; Sener, GNontraumatic psychological water avoidance stress has been shown to induce mucosal. degeneration, inflammatory cell infiltration and mast cell degranulation in stomach, ileum, colon and urinary bladder. Many skin disorders, such as atopic dermatitis and psoriasis, worsen during stress and seem to be related with infiltration and activation of mast cells releasing vasoactive and proinflammatory mediators. Melatonin is a free radical scavenger and has cytoprotective effects in inflammatory conditions. The aim of the present study was to investigate the effects of melatonin on water avoidance stress (WAS)-induced degranulation of mast cells in the dermis. Wistar rats were exposed to acute WAS (aWAS group) or chronic WAS (cWAS group). Before exposing to acute WAS, one group of animals was treated with 10mg/kg metatonin (aWAS+mel. group). In the cWAS+mel group, treatment with melatonin lasted for 5 days. Dermal mast cells were stained with toluidine blue and investigated using light microscopy. Numbers of mast cells were increased in both aWAS and cWAS groups, but numbers of degranulated mast cells were increased significantly only in the cWAS group when compared to the control group. Numbers of mature granulated and degranulated mast cells were decreased in the cWAS+mel. group when compared to the cWAS group. In conclusion, chronic metatonin treatment reduced WAS-induced infiltration and activation of mast cells in dermis and may provide a useful therapeutic option in stress-induced skin disorders. (c) 2004 Elsevier GmbH. All rights reserved.Publication Metadata only Oxytocin ameliorates oxidative colonic inflammation by a neutrophil-dependent mechanism(ELSEVIER SCIENCE INC, 2005) YEGEN, BERRAK; Iseri, SO; Sener, G; Saglam, B; Gedik, N; Ercan, F; Yegen, BCOxytocin (OT), a nonapeptide produced in the paraventricular and the supraoptical nuclei in the hypothalamus has a wide range of effects in the body. However, the role of OT on the gastrointestinal (GI) tract has to be settled. OT may participate in the regulation of motility, secretion, blood flow, cell turnover and release of neurotransmitters and/or peptides in the GI tract, possesses antisecretory and antiulcer effects, facilitates wound healing and is involved in the modulation of immune and inflammatory processes. The present work was conducted to assess the possible therapeutic effects of OT against the acetic acid-induced colonic injury in the rat. Methods: Colitis was induced by intracolonic administration of acetic acid (5%) in Sprague-Dawley rats (200-250 g). Either saline or OT (0.5 mg/kg) was injected subcutaneously, immediately after the induction of colitis and repeated two times a day for 4 days. On the 4th day, rats were decapitated and distal 8 cm of the colon were removed for the macroscopic and microscopic damage scoring, determination of tissue wet weight index (Wl), malondialdehyde (NIDA) levels, an end product of lipid peroxidation; glutathione (GSH) levels, a key antioxidant; and myeloperoxidase (MPO) activity, as an indirect index of neutrophil infiltration. Colonic collagen content, as a fibrosis marker was also determined. Lactate deydrogenase (LDH) and tumor necrosis factor-alpha (TNF-alpha) levels were assayed in serum samples. In the acetic acid-induced colitis, macroscopic and microscopic damage scores, WI, MDA and MPO levels were significantly increased, while GSH levels were decreased when compared to control group (p < 0.05-<0.001). Treatment with OT abolished the colitis-induced elevations in damage scores, WI, MDA and MPO levels and restored the GSH levels (p<0.05-0.001). Similarly. acetic acid increased the collagen content of colonic tissues and OT-treatment reduced this value to the level of the control group. Serum LDH and TNF-a levels were also elevated in the acetic acid-induced colitis group as compared to control group, while this increase was significantly decreased by OT treatment. The results suggest that OT, which improves the antioxidative state of the colonic tissue and ameliorates oxidative colonic injury via a neutrophil-dependent mechanism, requires further investigation as a potential therapeutic agent in colonic inflammation. (C) 2004, Elsevier Inc. All rights reserved.Publication Metadata only Melatonin protects against oxidative organ injury in a rat model of sepsis(SPRINGER, 2005) YEGEN, BERRAK; Sener, G; Toklu, H; Kapucu, C; Ercan, F; Erkanli, G; Kacmaz, A; Tilki, M; Yegen, BCPurpose. Based on the potent antioxidant effects of melatonin, we investigated the putative protective role of melatonin against sepsis-induced oxidative organ damage in rats. Methods. Sepsis was induced by cecal ligation and puncture (CLP) in Wistar albino rats. Animals subjected to CLP and sham-operated control rats were given saline or melatonin 10 mg/kg intraperitoneally 30 min before and 6 h after the operation. The rats were killed 16 h after the operation and the biochemical changes were investigated in the liver, kidney, heart, lung, diaphragm, and brain tissues by examining malondialdehyde (MDA) and glutathione (GSH) levels, and myeloperoxidase (MPO) activity. We also examined the tissues microscopically. Results. Sepsis resulted in a significant decrease in GSH levels and a significant increase in MDA levels and MPO activity (P < 0.05-P < 0.001) showing oxidative damage, which was confirmed by histological examination. Melatonin clearly reversed these oxidant responses and the microscopic damage, demonstrating its protective effects against sepsis-induced oxidative organ injury. Conclusion. The increase in MDA levels and MPO activity and the concomitant decrease in GSH levels demonstrate the role of oxidative mechanisms in sepsis-induced tissue damage. Melatonin, by its free radical scavenging and antioxidant properties, ameliorated oxidative organ injury. Thus, supplementing antiseptic shock treatment with melatonin may be beneficial in the clinical setting.Publication Metadata only Protective effect of beta-glucan against oxidative organ injury in a rat model of sepsis(ELSEVIER, 2005) ERCAN, FERİHA; Sener, G; Toklu, H; Ercan, F; Erkanli, GSepsis leads to various organ damage and dysfunction. One of the underlying mechanisms is thought to be the oxidative damage due to the generation of free radicals. In this study, we investigated the putative protective role of beta-gluican against sepsis-induced oxidative organ damage. Sepsis was induced by caecal ligation and puncture (CLP) in Wistar albino rats. Sham operated (control) and sepsis groups received saline or beta-glucan (50 mg/kg, po) once daily for 10 days and 30 min prior to and 6 h after the CLP. Sixteen hours after the surgery, rats were decapitated and the biochemical changes were determined in the brain, diaphragm, kidney, heart, liver and lung tissues using malondialdehyde (N4DA) content - an index of lipid peroxidation - glutathione (GSH) levels - a key antioxidant - and myeloperoxidase (MPO) activity - an index of neutrophil infiltration. Serum TNF-alpha levels were assessed by RIA method. Tissues were also examined under light microscope to evaluate the degree of sepsis-induced damage. The results demonstrate that sepsis significantly decreased GSH levels and increased the MDA levels and MPO activity (p < 0.05-p < 0.001) causing oxidative damage. Elevated plasma TNF-alpha levels in septic rats significantly reduced to control levels in beta-glucan treated rats. Since -glucan administration reversed these oxidant responses, it seems likely that beta-glucan protects against sepsis-induced oxidative organ injury. (c) 2005 Elsevier B.V. All rights reserved.Publication Metadata only Taurine ameliorates stress-induced degeneration of the urinary bladder(ELSEVIER GMBH, URBAN & FISCHER VERLAG, 2007) ERCAN, FERİHA; Zeybek, Ali; Saglam, Beyhan; Cikler, Esra; Cetinel, Sule; Ercan, Feriha; Sener, GokselWe studied the potential effects of taurine, a free radical scavenger, on chronic water avoidance stress (WAS)-induced degeneration of the mucosa of the urinary bladder in experimental rats. Wistar albino rats were exposed to WAS for 2 h/day, for 5 days (WAS group). Before exposing them to WAS, taurine (50 mg/kg) (WAS+taurine group) was injected intraperitonally into the animals. Samples of urinary bladder were then investigated by light and scanning electron microscopy. Lipid peroxidation and gluthathione levels were also measured in the urinary bladder. In the WAS-only group, inflammatory cell infiltration, increased number of mast cells in the mucosa and ulcerated areas were observed. In the WAS+taurine group, relatively normal urothelial topography with microvilli, moderate inflammatory cell infiltration and decreased numbers of mast cells in the mucosa were observed. The increased lipid peroxidation and decreased glutathione levels in WAS rats were reversed by taurine treatment. We conclude that taurine protects against WAS-induced oxidant urinary bladder injury, and thus may be a possible therapeutic agent against interstitial cystitis, the symptoms of which are aggravated by stress conditions. (c) 2006 Elsevier GmbH. All rights reserved.Publication Open Access Protective effects of quercetin against cisplatin induced urogenital organ toxicity(MARMARA UNIV, 2020-09-11) ERCAN, FERİHA; Sener, Tarik Emre; Cadirci, Selin; Cevik, Ozge; Ercan, Feriha; Koroglu, M. Kutay; Sakarcan, Selin; Sener, GokselCisplatin is a chemotherapeutic agent that is the first to enter treatment from organic platinum-derived drugs. Nephrotoxicity and cytotoxicity are major factors that limit its use. The aim of the study is to investigate the possible protective effects of quercetin against cisplatin-induced urogenital organ toxicity. In our study, Sprague Dawley four month old male rats were divided into 4 groups; control + saline (SF), control + quercetin (20 mg/kg for 21 days), cisplatin (7 mg/kg as a single dose) + SF and cisplatin + quercetin groups. After decapitation, the kidney, bladder, testis and corpus cavernosum tissue samples were taken to analyze caspase-3, an index of apoptosis, and oxidative stress parameters such as malondialdehyde (MDA), gluta-thione (GSH), and 8-hydroxy-2'-deoxyguanosine (8-OHdG). Furthermore, tissues were also examined histologically. Cisplatin caused significant increases in MDA and 8-OHdG levels, demonstrating increases in lipid peroxidation and oxidative DNA damage, respectively, in all tissues. In parallel with the oxidant stress increase, the endogenous strong antioxidant GSH levels were decreased. Caspase activity and caspase 3 expressions, which we measured as an indicator of apoptosis, increased significantly with cisplatin treatment. On the other hand, treatment with quercetin, a powerful antioxidant flavonoid, reversed these changes. Histological findings also demonstrated well-preserved tissues due to quercetin treatment. In conclusion, our results suggested that quercetin, when given with cisplatin, can be protective against the chemotherapeutic induced toxicity and thus provide therapeutic benefit.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.