Person: ERCAN, FERİHA
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ERCAN
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FERİHA
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Publication Metadata only L-Carnitine ameliorates methotrexate-induced oxidative organ injury and inhibits leukocyte death(SPRINGER, 2006) YEGEN, BERRAK; Sener, G; Eksioglu-Demiralp, E; Cetiner, M; Ercan, F; Sirvanci, S; Gedik, N; Yegen, BCMethotrexate (MTX), a folic acid antagonist widely used for the treatment of a variety of tumors and inflammatory diseases, affects normal tissues that have a high rate of proliferation, including the hematopoietic cells of the bone marrow and the gastrointestinal mucosal cells. To elucidate the role of free radicals and leukocytes in MTX-induced oxidative organ damage and the putative protective effect of L-carnitine (L-Car), Wistar albino rats were administered a single dose of MTX (20 mg/kg) followed by either saline or L-Car (500 mg/kg) for 5 days. After decapitation of the rats, trunk blood was obtained, and the ileum, liver, and kidney were removed for histological examination and for the measurement of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity, and collagen content. Our results showed that MTX administration increased the MDA and MPO activities and collagen content and decreased GSH levels in all tissues, while these alterations were reversed in L-Car-treated group. The elevated serum TNF-alpha level observed following MTX treatment was depressed with L-Car. The oxidative burst of neutrophils stimulated by Annexin V was reduced in the saline-treated MTX group, while L-Car abolished this inhibition. Similarly, flow cytometric measurements revealed that leukocyte apoptosis was increased in MTX-treated animals, while L-Car reversed these effects. Severe degeneration of the intestinal mucosa, liver parenchyma, and glomerular and tubular epithelium observed in the saline-treated MTX group was improved by L-Car treatment. These results suggest that L-Car, possibly via its free radical scavenging and antioxidant properties, ameliorates MTX-induced oxidative organ injury and inhibits leukocyte apoptosis. Thus, supplementation with L-Carnitine as an adjuvant therapy may be promising in alleviating the systemic side-effects of chemotherapeutics.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 Taurine protects against methotrexate-induced toxicity and inhibits leukocyte death(ACADEMIC PRESS INC ELSEVIER SCIENCE, 2005) YEGEN, BERRAK; Cetiner, M; Sener, G; Sehirli, AO; Eksioglu-Demiralp, E; Ercan, F; Sirvanci, S; Gedik, N; Akpulat, S; Tecimer, T; Yegen, BCThe efficacy of methotrexate (MTX), a widely used cytotoxic chemotherapeutic agent, is often limited by severe side effects and toxic sequelae. Regarding the mechanisms of these side effects, several hypotheses have been put forward, among which oxidative stress is noticeable. The present study was undertaken to determine whether taurine, a potent free radical scavenger, could ameliorate MTX-induced oxidative injury and modulate immune response. Following a single dose of methotrexate (20 mg/kg), either saline or taurine (50 mg/kg) was administered for 5 days. After decapitation of the rats, trunk blood was obtained and the ileum, liver, and kidney were removed to measure malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity, and collagen content, as well as histological examination. Our results showed that MTX administration increased the MDA, MPO activity, and collagen contents and decreased GSH levels in all tissues (P < 0.001), while these alterations were reversed in taurine-treated group (P < 0.05-0.01). Elevated (P < 0.001) TNF-alpha level observed following MTX treatment was depressed with taurine (P < 0.01). Oxidative burst of neutrophils stimulated by phorbol myristate acetate was reduced in saline-treated MTX group (P < 0.001), while taurine abolished this effect. Similarly, flow cytometric measurements revealed that leukocyte apoptosis and cell death were increased in MTX-treated animals, while taurine reversed these effects (P < 0.05). Reduced cellularity in bone marrow samples of MTX-treated group (P < 0.01) was reversed back to control levels in taurine-treated rats. Severe degeneration of the intestinal mucosa, liver parenchyma, glomerular, and tubular epithelium observed in saline-treated group was improved by taurine treatment. In conclusion, it appears that taurine protects against methotrexate-induced oxidant organ injury and inhibits leukocyte apoptosis and may be of therapeutic potential in alleviating the systemic side effects of chemotherapeutics. (c) 2005 Published by Elsevier Inc.Publication Metadata only High cholesterol diet activates ER stress mediated apoptosis in testes tissue: Role of alpha-tocopherol(WILEY) SÖZEN, AHMET ERDİ; Sozen, Erdi; Demirel-Yalciner, Tugce; Koroglu, M. Kutay; Elmas, Merve Acikel; Ercan, Feriha; Ozer, Nesrin KartalThe seminiferous tubules where spermatogenesis occurs are enveloped and protected by the Sertoli cells to support germ cells undergoing meiosis to produce haploid gametes. Clearly, induction of apoptosis in seminiferous tubules leads to abnormalities in spermatogenesis and male infertility. Studies demonstrated that increased hyperlipidemia impairs male infertility and spermatogenesis by enhancing seminiferous tubules apoptosis. However, molecular mechanisms underlying high-cholesterol-mediated testicular damage remain poorly elucidated. In this scope, we established a rabbit model and investigated the role of endoplasmic reticulum (ER) stress on high cholesterol diet induced seminiferous tubule apoptosis. Histopatological examinations revealed increased seminifer tubule apoptosis in testes of rabbits fed high cholesterol diet. In addition, phosphorylated forms of IRE1 and PERK, two well-identified markers of ER stress, were significantly induced in accordance with high cholesterol diet. High cholesterol diet also exhibited CHOP induction in testes, indicating increased ER stress related apoptosis. Supplementation of alpha-tocopherol significantly attenuated cholesterol mediated ER stress, and restored seminiferous tubules apoptosis. Taken together, our findings suggest that alpha-tocopherol might be capable to reduce testicular damage via ameliorating histopatological features and inhibiting seminiferous tubules apoptosis in hypercholesterolemic rabbits.Publication Open Access Resveratrol treatment reduces apoptosis and morphological alterations in cisplatin induced testis damage(MARMARA UNIV, 2019-07-15) ERCAN, FERİHA; Ozyilmaz Yay, Nagehan; Sener, Goksel; Ercan, FerihaCisplatin commonly used as a chemotheropotic agent however, it is associated with numerous side effects such as reproductive cytotoxicity. It causes spermatogenic cell death and DNA damage in spermatozoa via the formation of reactive oxygene species. Resveratrol (3,5,4'-trans-trihydroxystilbene), a natural phytoalexin, is a potent antioxidant agent, present in a wide variety of dietary sources including grapes, plums and peanuts. The aim of present study to evaluate the beneficial effects of resveratrol on cisplatin induced testis damage. Male Sprague Dawley rats were used in the study and four experimental groups were formed as: 1- saline applied control, 2- resveratrol applied control, 3- cisplatin and 4- cisplatin+resveratrol groups. Following a single dose of cisplatin (7 mg/kg i.p.), either saline or resveratrol (10 mg/kg, orally) was administered for 5 days. Testis samples were prepared for histopathological and ultrastructural evaluations, cell proliferation and apoptosis. Tissue malondialdehyde (MDA), glutathione (GSH) levels and myeloperoxidase (MPO) activity were determined biochemically. Degenerated and atrophic tubules of tissue, apoptotic cells, MDA level and MPO activity were increased although proliferation index and GSH level were decreased in cisplatin group. Degenerated tight junctions between the Sertoli cells and vacuole formation in germinal epithelial cells were also revealed at this group. However, resveratrol treatment reduced degenerated and atrophic tubules, apoptotic cells, vacuole formation in germinal epithelial cells, MDA level and MPO activity and increased proliferation index and GSH level in testis. These results showed that resveratrol ameliorates cisplatin induced testis injury by the impairment of oxidative stress and apoptosis.Publication Open Access Betulinic Acid Protects against Ischemia/Reperfusion-induced Renal Damage and Inhibits Leukocyte Apoptosis(WILEY, 2010-03) ERCAN, FERİHA; Eksioglu-Demiralp, Emel; Kardas, E. Riza; Ozgul, Seckin; Yagci, Tayfur; Bilgin, Hueseyin; Sehirli, Oezer; Ercan, Feriha; Sener, GoekselThe possible protective effect of betulinic acid on renal ischemia/reperfusion (I/R) injury was studied. Wistar Albino rats were unilaterally nephrectomized and subjected to 45 min of renal pedicle occlusion followed by 6 h of reperfusion. Betulinic acid (250 mg/kg, i.p.) or saline was administered at 30 min prior to ischemia and immediately before the reperfusion. Creatinine, blood urea nitrogen (BUN), lactate dehydrogenase (LDH) and TNF-alpha as well as the oxidative burst of neutrophil and leukocyte apoptosis were assayed in blood samples. Malondialdehyde (MDA), glutathione (GSH) levels, Na+, K+-ATPase and myeloperoxidase (MPO) activities were determined in kidney tissue which was also analysed microscopically. I/R caused significant increases in blood creatinine, BUN, LDH and TNF-alpha. In the kidney samples of the I/R group, MDA levels and MPO activity were increased significantly, however, GSH levels and Na+, K+-ATPase activity were decreased. Betulinic acid ameliorated the oxidative burst response to both formyl-methionyl-leucyl-phenylalanine (fMLP) and phorbol 12-myristate 13-acetate (PMA) stimuli, normalized the apoptotic response and most of the biochemical indices as well as histopathological alterations induced by I/R. In conclusion, these data suggest that betulinic acid attenuates I/R-induced oxidant responses, improved microscopic damage and renal function by regulating apoptotic function of leukocytes and inhibiting neutrophil infiltration. Copyright (C) 2009 John Wiley & Sons, Ltd.Publication Open Access Distribution of Zonula Occludens-1 and Occludin and alterations of testicular morphology after in utero radiation and postnatal hyperthermia in rats(WILEY, 2012-12) ERCAN, FERİHA; Senturk, Gozde Erkanli; Canillioglu, Yasemin Ersoy; Umay, Cenk; Demiralp-Eksioglu, Emel; Ercan, FerihaIn utero irradiation (IR) and postnatal hyperthermia (HT) exposure cause infertility by decreasing spermatogenic colony growth and the number of sperm in rats. Four groups were used: (i) Control group, (ii) HT group (rats exposed to hyperthermia on the 10th postnatal day), (iii) IR group (rats exposed to IR on the 17th gestational day) and (iv) IR + HT group. Three and six months after the procedures testes were examined by light and electron microscopy. Some degenerated tubules in the HT group, many vacuoles in spermatogenic cells and degenerated tight junctions in the IR group, atrophic tubules and severe degeneration of tight junctions in the IR + HT group were observed. ZO-1 and occludin immunoreactivity were decreased and disorganized in the HT and IR groups and absent in the IR + HT group. The increase in the number of apoptotic cells was accompanied by a time-dependent decrease in haploid, diploid and tetraploid cells in all groups. Degenerative findings were severe after 6 months in all groups. The double-hit model may represent a Sertoli cell only model of infertility due to a decrease in spermatogenic cell and alterated blood-testis barrier proteins in rat.Publication Open Access Apocynin ameliorates testicular toxicity in high-fat diet-fed rats by regulating oxidative stress(2023-03-01) ERTAŞ, BÜŞRA; ERCAN, FERİHA; Hersek İ., Coşkunlu B., Köroğlu M., Ertaş B., Şener G., Ercan F.Objective: The purpose of this study was to examine the effects of apocynin (APC), an inhibitor of NADPH oxidase (NOX), on high-fat diet (HF)-induced testis cytotoxicity.Methods: Wistar albino rats were divided into three groups as control, HF and HF+APC groups. Rats in HF and HF+APC groups were fed using HFfor 16 weeks and in the last four weeks of this period vehicle solution or APC (25 mg/kg) was administered orally five days a week, respectively.Control group was fed with standart lab chow for 16 weeks. Cholesterol, triglyceride, high-density lipoproteins, leptin, estrogen, testosterone,LH and FSH were estimated in blood serum. Sperm parameters were analysed from the epididymis. Testicular malondialdehyde, 8‐hydroxy‐2‐deoxyguanosine, glutathione, superoxide dismutase and myeloperoxidase levels were estimated biochemically. Testicular morphology,proliferative, apoptotic and NOX2-positive cells were analysed histologically.Results: HF-induced obesity caused significant alterations in serum lipid and hormone profiles. Testicular malondialdehyde, 8‐hydroxy‐2‐deoxyguanosine, and myeloperoxidase levels increased, glutathione and superoxide dismutase levels decreased in this group. Moreover,altered sperm parameters, increased degenerated seminiferous tubules, apoptotic and NOX2 – positive cells and decreased proliferative cellswere observed in the HF group. All these biochemical and histological alterations improved in the HF+APC group.Conclusion: HF-induced obesity causes altreations in lipid values, sperm parameters and testicular morphology by increasing oxidative stressthrough NOX2 activity. Apocynin might prevent testis damage via regulating oxidant/antioxidant balance.Publication Metadata only Apocynin alleviates cisplatin-induced testicular cytotoxicity by regulating oxidative stress and apoptosis in rats(WILEY, 2019) ERCAN, FERİHA; Koroglu, Kutay M.; Cevik, Ozge; Sener, Goksel; Ercan, FerihaThe aim of this study was to investigate possible protective effects of apocynin (APO), an NADPH oxidase (NOX2) inhibitor, on cisplatin (CIS)-induced testicular damage. Four groups of Sprague Dawley rats were used: control, APO, CIS and CIS+APO. Following a single intraperitoneal dose of CIS (7 mg/kg), either dimethyl sulfoxide or APO (25 mg/kg) was administered orally for 5 days. Testis samples were evaluated microscopically for general histopathology and ultrastructure, proliferating and apoptotic cells, and NOX2 localization. Sperm parameters were evaluated. Malondialdehyde (MDA) and glutathione (GSH) levels and superoxide dismutase (SOD), myeloperoxidase (MPO) and 8-hydroxy-2-deoxyguanosine (8-OHdG) activities were analysed biochemically. The CIS group had a greater number of abnormal spermatozoa, atrophic seminiferous tubules, apoptotic and NOX2-immunoreactive cells; numerous large vacuole formations in the cytoplasm of germinal epithelial cells; degenerated intercellular tight junctions; higher MDA, 8-OHdG and MPO levels; decreased numbers of spermatozoa; and lower proliferative index and GSH and SOD levels. All these histologic and biochemical results were better in the CIS+APO group. CIS causes testicular damage by decreasing spermatogenic cell lines and increasing NOX2 activity and apoptosis through oxidative stress. APO prevents testicular damage, possibly by its antioxidant effects.Publication Metadata only beta-glucan ameliorates methotrexate-induced oxidative organ injury via its antioxidant and immunomodulatory effects(ELSEVIER, 2006) YEGEN, BERRAK; Sener, Goksel; Eksioglu-Demiralp, Emel; Cetiner, Mustafa; Ercan, Feriha; Yegen, Berrak C.Methotrexate is an antifolate that is widely used in the treatment of rheumatic disorders and malignant tumors. The efficacy of methotrexate is often limited by severe side effects and toxic sequelae, where oxidative stress is noticeable. In the present study, the possible protective effect of beta-glucan in methotrexate-induced toxicity was investigated. Following a single dose of methotrexate injection (20 mg/kg), either saline or beta-glucan (50 mg/kg; orally) was administered for 5 days. After decapitation of the rats, trunk blood was obtained and the ileum, liver and kidney were removed to measure tissue malondialdehyde (NMA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity and collagen content, as well as histological examination. Methotrexate caused a significant decrease in GSH levels, while MDA levels, WO activity and collagen content were increased in all the tissues (P < 0.05-0.001). On the other hand, administration of IS-glucan following methotrexate abolished the depletion of GSH and inhibited the increases in MDA, MPO activity and collagen content, while the histological analysis revealed that beta-glucan attenuated the tissue damage. Stimulation index, an indicator of oxidative burst in the neutrophils, was decreased by methotrexate (P < 0.001), while beta-glucan abolished this effect. Furthermore, increased leukocyte apoptosis and cell death in methotrexate-treated animals were inhibited by beta-glucan (P < 0.05). Thus, the findings of the present study suggest that beta-glucan, through its antioxidant and immunoregulatory effects, may be of therapeutic value in alleviating the leukocyte apoptosis, oxidative tissue injury and thereby the intestinal and hepatorenal side effects of methotrexate treatment. (c) 2006 Elsevier B.V. All rights reserved.