Person: ERCAN, FERİHA
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ERCAN
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FERİHA
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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 anti-inflammatory effect of leptin on experimental colitis: involvement of endogenous glucocorticoids(ELSEVIER SCIENCE INC, 2004) YEGEN, BERRAK; Cakir, B; Bozkurt, A; Ercan, F; Yegen, BCThe present study was designed to compare the effect of leptin on acute colonic inflammation with that of acute stress exposure, which acts via the hypothalamic-pituitary-adrenal (HPA) axis. Sprague-Dawley rats of both sexes were administered intrarectally with acetic acid. Either leptin (10 mug/kg; i.p.) or saline was injected immediately before and 6 h after the induction of colitis. A group of rats was exposed to water avoidance stress (WAS) for 30 min at the 6th h of colitis induction. RU-486 (2 mg/kg; i.p.), a glucocorticoid receptor antagonist, was injected intraperitoneally, at 12 and 1 h before the initial leptin injection, and at 1 h before the second leptin injection or exposure to WAS. Rats were decapitated at 24 h and the distal 8 cm of,the colon were removed for macroscopic and microscopic scoring, determination of tissue wet weight index (WI) and tissue myeloperoxidase activity (MPO). Acetic acid-induced colitis significantly increased macroscopic and microscopic damage scores, WI and MPO, compared to control group. Exposure to acute WAS or treatment with leptin reduced the elevations in damage scores, WI and MPO induced by colitis, but no additive inhibitory effect was observed when WAS and leptin were applied together. RU-486 treatment reversed the inhibitory effects of leptin or WAS on colonic inflammation. Our results demonstrate that exogenous leptin mimics the effects of HPA axis activation on colitis-induced inflammatory process. The results also suggest that the anti-inflammatory effect of leptin involves a tissue neutrophil-dependent mechanism and is dependent on the release of glucocorticoids. (C) 2003 Elsevier Inc. All rights reserved.Publication Metadata only Resveratrol alleviates bleomycin-induced lung injury in rats(ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD, 2007) ERCAN, FERİHA; Sener, Goksel; Topaloglu, Nurhayat; Sehirli, A. Ozer; Ercan, Feriha; Gedik, NursalAntioxidant therapy may be useful in diseases with impaired oxidant-antioxidant balance such as pulmonary fibrosis. This study was designed to examine the effects of resveratrol, an antioxidant agents, against bleomycin-induced pulmonary fibrosis and oxidative damage. Wistar albino rats were administered a single dose of bleomycin (5 mg/kg; via the tracheal cannula) followed by either saline or resveratrol (10 mg/kg; orally) for 14 days. The effect of resveratrol on pulmonary oxidative damage was studied by cell count and analysis of cytokine levels (TGF-beta, TNF-alpha, IL-1 beta and IL-6) in the bronchoalveolar lavage fluid (BALF) and biochemical measurements of malondialdehyde (MDA), an end product of lipid peroxidation; glutathione (GSH), a key antioxidant; and myeloperoxidase (MPO) activity, an index of neutrophil infiltration, in the lung tissue. Bleomycin-induced lung fibrosis was determined by lung collagen contents and also microscopically. Bleomycin caused a significant decrease in lung GSH, which was accompanied with significant increases in MDA level, MPO activity, and collagen contents of the lung tissue concomitant with increased levels of the pro-inflammatory mediators and cell count in BALF. On the other hand, resveratrol treatment reversed all these biochemical indices as well as histopathological alterations induced by bleomycin. The results demonstrate the role of oxidative mechanisms in bleomycin-induced pulmonary fibrosis, and resveratrol, by its antioxidant properties, ameliorates oxidative injury and fibrosis due to bleomycin. Thus, an effective supplement with resveratrol as an adjuvant therapy may be a very promising agent in alleviating the side effects of bleomycin, an effective chemotherapeutic agent. (C) 2006 Elsevier Ltd. All rights reserved.Publication Metadata only Alpha-lipoic acid protects against hepatic ischemia-reperfusion injury in rats(KARGER, 2007) DULUNDU, ENDER; Dulundu, Ender; Ozel, Yahya; Topaloglu, Umit; Sehirli, Ozer; Ercan, Feriha; Gedik, Nursal; Sener, GokselBackground and Aim: To evaluate the protective effect of alpha-lipoic acid in reducing oxidative damage after severe hepatic ischemia/reperfusion (IR) injury. Methods: Wistar albino rats were subjected to 45 min of hepatic ischemia, followed by 60 min reperfusion period. Lipoic acid (100 mg/kg i.p.) was administered 15 min prior to ischemia and immediately before reperfusion period. At the end of the reperfusion period aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH) activity, and cytokine, TNF-alpha and IL-1 beta levels were determined in serum samples. Malondialdehyde (MDA), and glutathione (GSH) levels and myeloperoxidase (MPO) activity were determined in the liver tissue samples while formation of reactive oxygen species was monitored by using chemiluminescence ( CL) technique with luminol and lucigenin probes. Tissues were also analyzed histologically. Results: Serum ALT, AST, and LDH activities and TNF-alpha and IL-1 beta levels were elevated in the I/R group, while this increase was significantly lower in the group of animals treated concomitantly with lipoic acid. Hepatic GSH levels, significantly depressed by I/R, were elevated back to control levels in lipoic acid-treated I/R group. Furthermore, increases in tissue luminol and lucigen-in CL, MDA levels and MPO activity due to I/R injury were reduced back to control levels with lipoic acid treatment. Conclusion: Since lipoic acid administration alleviated the I/R-induced liver injury and improved the hepatic structure and function, it seems likely that lipoic acid with its antioxidant and oxidant-scavenging properties may be of potential therapeutic value in protecting the liver against oxidative injury due to ischemia-reperfusion. Copyright (c) 2007 S. Karger AG, Basel.Publication Metadata only Propylthiouracil (PTU)-induced hypothyroidism alleviates burn-induced multiple organ injury(ELSEVIER SCI LTD, 2006) VELİOĞLU ÖĞÜNÇ, AYLİZ; Sener, Goeksel; Sehirli, Oezer; Velioglu-Oeguenc, Ayliz; Ercan, Feriha; Erkanli, Goezde; Gedik, Nursal; Yegen, Berrak C.Oxidative stress has an important role in the development of multiorgan failure after major burn. This study was designed to determine the possible protective effect of experimental hypothyroidism in hepatic and gastrointestinal injury induced by thermal trauma. Sprague Dawley rats were administered saline or PTU (10 mg kg(-1) i.p.) for 15 days, and hypothyroidism was confirmed by depressed serum T-3 and T-4 concentrations. Under brief ether anesthesia, shaved dorsurn of rats was exposed to 90 degrees C (burn group) or 25 degrees C (control group) water bath for 10 s. PTU or saline treatment was repeated at the 12th hour of the burn. Rats were decapitated 24 h after injury and tissue samples from liver, stomach and ileum were taken for the determination of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity and collagen contents. Formation of reactive oxygen species in tissue samples was monitored by using chemiluminescence (CL) technique with luminol and lucigenin probes. Tissues were also examined microscopically. Tumor necrosis factor (TNF)-alpha and lactate dehydrogenase (LDH) were assayed in serum samples. Severe skin scald injury (30% of. total body surface area) caused a significant decrease in GSH level, which was accompanied with significant increases in NIDA level, MPO activity, CL levels and collagen content of the studied tissues (p < 0.05-0.001). Similarly, serum TNF-alpha and LDH were elevated in the burn group as compared to control group. On the other hand, PTU treatment reversed all these biochemical indices, as well as histopathological alterations induced by thermal trauma. Our results suggest that PTU-induced hypothyroidism reduces oxidative damage in the hepatic, gastric and ileal tissues probably due to hypometabolism, which is associated with decreased production of reactive oxygen metabolites and enhancement of antioxidant mechanisms. (C) 2006 Elsevier Ltd and ISBI. All rights reserved.Publication Open Access Grape seed extract treatment reduces hepatic ischemia-reperfusion injury in rats(JOHN WILEY & SONS LTD, 2008-01) DULUNDU, ENDER; Sehirli, Ozer; Ozel, Yahya; Dulundu, Ender; Topaloglu, Umit; Ercan, Feriha; Sener, GokselThis study was designed to determine the possible protective effect of grape seed extract (GSE), a widely used antioxidant dietary supplement, on hepatic ischemia/reperfusion (I/R) injury. Wistar albino rats were subjected to 45 min of hepatic ischemia, followed by a 60 min reperfusion period. GSE was administered in a dose of 50 mg/kg/day orally for 15 days before (I/R) injury and repeated before the reperfusion period. Liver samples were taken for histological examination or determination of hepatic malondialdehyde (MDA), glutathione (GSH) and myeloperoxidase (MPO) activity. Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels were determined to assess liver functions. Lactate dehydrogenase (LDH) and cytokines (TNF-alpha and IL-1 beta) were also assayed in serum samples for the evaluation of generalized tissue damage. Ischemia/reperfusion caused a significant decrease in hepatic GSH, and significant increases in MDA level, and MPO activity. Serum AST and ALT levels, as well as LDH activity and plasma TNF-alpha and IL-1 beta levels were also elevated in the I/R group. Treatment with GSE reversed all these biochemical parameters as well as histological alterations induced by I/R. In conclusion, GSE reduced I/R-induced organ injury through its ability to balance the oxidant-antioxidant status, to inhibit neutrophil infiltration and to regulate the release of inflammatory mediators. Copyright (c) 2007 John Wiley & Sons, Ltd.Publication Metadata only Role of melatonin in reducing water avoidance stress-induced degeneration of the liver(SPRINGER, 2005) ERCAN, FERİHA; Contuk, G; Ercan, F; Cetinel, S; Cikler, E; Sener, GMelatonin, a pineal secretory product, is a potent scavenger of a variety of free radicals. We investigated the role of melatonin on water avoidance stress (WAS)-induced degenerations of the liver parenchyme. Wistar albino rats were exposed to acute WAS (aWAS group) or chronic WAS (cWAS group). Before exposing animals to acute (aWAS + mel group) or chronic WAS (cWAS + mel group), 10 mg/kg melatonin was injected i.p. The liver samples were investigated under light and transmission electron microscope. Malondialdehyde (MDA) and glutathione (GSH) levels were also determined. Prominent vascular congestion and dilated sinusoids, activated Kupffer cells with prominent morphology, dilated granular endoplasmic reticulum membranes, and focal picnotic nuclei were observed in the aWAS group; these morphological changes were severe in the cWAS group. MDA level was increased and GSH level was decreased significantly in the cWAS group. The morphology of liver parenchme in both the aWAS + mel and the cWAS + mel group showed that melatonin significantly reduced the degeneration in liver; besides, a significant decrease in MDA and an increase in GSH levels were observed in the cWAS + mel group. Based on the results, melatonin treatment significantly prevented WAS-induced morphological and biochemical changes in liver parenchyma.Publication Metadata only Aqueous garlic extract inhibits protamine sulfate-induced bladder damage(KARGER, 2006) ERCAN, FERİHA; Zeybek, A; Cikler, E; Saglam, B; Ercan, F; Cetinel, S; Sener, GThis morphological and biochemical study aims to investigate the antioxidant effects of chronic administration of aqueous garlic extract (AGE) on protamine sulfate (PS)-induced bladder injury. Wistar albino female rats were catheterized and intravesically infused with phosphate-buffered solution (control group) or PS (PS group) dissolved in phosphate-buffered solution. In the PS + AGE group after the PS instillation, AGE (1 ml/kg, i. p., corresponding to 250 mg/kg) was injected intraperitoneally for 3 days. Bladder morphology was investigated by light and scanning electron microscopy. Tissue samples were also obtained to determine bladder malondialdehyde (MDA) and glutathione levels. In the PS group, ulcerated areas, an irregular mucus layer, inflammatory cell infiltration and an increased number of mast cells were observed. In the PS + AGE group a relatively normal urothelial topography, glycosaminoglycan layer and a decreased number of mucosal mast cells and inflammatory cells were observed. Increased MDA levels as a result of PS induction led us to propose that free radicals may have a critical role in this injury. The significant decrease in MDA and increase in glutathione levels in the PS + AGE group was in accordance with morphological findings. Based on the results, AGE treatment significantly prevented PS-induced degenerative morphological and biochemical changes of urinary bladder mucosa. Copyright (c) 2006 S. Karger AG, Basel.Publication Metadata only Leukotriene D4 receptor antagonist montelukast alleviates water avoidance stress-induced degeneration of the gastrointestinal mucosa(ELSEVIER SCI LTD, 2008) ERCAN, FERİHA; Ersoy, Yasemin; Cikler, Esra; Cetinel, Sule; Sener, Goekel; Ercan, FerihaWe investigated the role of montelukast (ML), a cysteinyl leukotriene-1 receptor antagonist, on the water avoidance stress (WAS)induced degeneration of the rat gastric, ileal and colonic mucosa. One group of Wistar albino rats were exposed to chronic WAS (WAS group) 2 h daily for 5 days. Another group was administered ML (10 mg/kg; i.p.; WAS + ML group) following every WAS exposure for 5 days. Control rats were injected with the vehicle solution only. The stomach, ileum and colon were dissected and investigated for histopathological changes with a light microscope as well as for topographical changes with a scanning electron microscope. The levels of malondialdehyde (MDA, a biomarker of oxidative damage) and glutathione (GSH, a biomarker of protective oxidative injury) were also determined in all dissected tissues. In the WAS group, the stomach epithelium showed ulceration in some areas, dilatations of the gastric glands, degeneration of gastric glandular cells, and prominent congestion of the capillaries. In a similar fashion, degenerated epithelium and severe vascular congestions were observed in the ileum and colon. In all the tissues dense inflammatory cell infiltration and mast cell degranulation in mucosa were observed. The levels of MDA were significantly increased whereas those of GSH were significantly decreased in all test tissues in the WAS group compared to the control group. The morphology of gastric, ileal and colonic mucosa in WAS + ML group showed a significant amelioration showing a reduction in inflammatory cell infiltration and mast cell degranulation. Increased NIDA and decreased GSH levels in the WAS group were also ameliorated with ML treatment. Based on the results, ML supplement seems attenuated inflammatory effects of WAS induction in gastrointestinal mucosa. (C) 2008 Elsevier Ltd. All rights reserved.Publication Metadata only LDH levels and left atrial ultrastructural chances in patients with mitral paraprosthetic regurgitation(WILEY, 2005) ERCAN, FERİHA; Mansuroglu, D; Omeroglu, SN; Izgi, A; Ercan, F; Yaymaci, B; Basaran, Y; Yakut, CBackground and aim: The aim of this study was to assess the effect of paraprosthetic regurgitation of mitral mechanical valves to myocardial tissue and lactate dehydrogenase (LDH) level. Methods: We compared 19 patients (study group) who had mitral mechanical valve with severe mitral paravalvular regurgitation with 20 patients (control group) who had native valve with severe rheumatic mitral regurgitation. None of the patients had clinical hemolytic anemia. On transesophageal echocardiographic examination, semiquantative evaluation and spatial distribution of regurgitant jets were noted in both of the groups. Five LDH isoenzymes were studied in two groups. Myocardial tissue specimens were taken from the left atrial wall during reoperation. Grids randomly taken were studied under the transmission electron microscope. Results: Total serum LDH levels of the study group (578 +/- 12 IU/L) were higher than the control group (495 +/- 6.2 IU/L) (p < 0.001). We found LDH1/LDH2 more than 1 in all patients; the ratio was not statistically different in the control group. Electron microscopy revealed the same degree of injury in both groups. Haptoglobin levels were decreased and reticulocyte counts were increased in patients with paraprosthetic valve regurgitation. Conclusions: Electron microscopic findings support that myocardial injury contributes to increase of total LDH level and high LDH1/LDH2 ratio. But statistically significant elevation in total LDH level in study group and the stable state of LDH1/LDH2 ratio between two groups showed that hemolysis caused by paraprosthetic regurgitation is the most important factor for the increase of total LDH level, so that high LDH level can be used as a reliable parameter for the diagnosis of intravascular hemolysis in paraprosthetic regurgitation.