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ERCAN, FERİHA

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ERCAN

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FERİHA

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Now showing 1 - 10 of 11
  • PublicationOpen Access
    Cerrahi menopoz oluşturulmuş sıçanların karaciğer ve böbrek dokularında oksidan/antioksidan dengenin korunmasında egzersizin ve östrojenin yararlı etkileri
    (2022-09-01) YÜKSEL, MERAL; ERCAN, FERİHA; YILDIRIM, ALPER; YEGEN, BERRAK; Tamer S. A. , Levent N., Yüksel M., Ercan F., Yıldırım A., Yegen B.
    Amaç: Bu çalışmanın amacı cerrahi olarak menopoz oluşturulan sıçanların böbrek ve karaciğerlerinde gözlenen histopatolojik ve fonksiyonel değişiklikleri ve östrojen veya egzersizin ya da östrojen-egzersiz kombinasyonunun oksidan hasar üzerine etkilerini araştırmaktır.Materyal ve Metot: Anestezi altında Sprague Dawley dişi sıçanlara (n=32) bilateral overiektomi uygulandı ve tüm sıçanlar rastgele olarak iki gruba ayrıldı. Sıçanların yarısına normal içme suyu, diğer yarısının içme sularına östrojen (1mg/kg/gün) eklendi. İki hafta sonra gruplar kendi içlerinde sedanter ve egzersiz (5 gün/hafta, 30 daki-ka, 8 hafta) gruplarına ayrıldı. Deney protokolünün sonun-da serum, karaciğer ve böbrek örnekleri biyokimyasal ve histopatolojik incelemeler için alındı. Femurda da histopa-tolojik değerlendirme yapıldı.Bulgular: Cerrahi olarak menopoz oluşturulan sıçan-larda östrojenin böbrek dokusunda nötrofil infiltrasyonunu ve reaktif oksijen türlerinin üretimini baskılayarak koruyu-cu etki gösterdiği, kemik kütlesinde hafif düzeyde artışa neden olduğu, ancak karaciğerin antioksidan glutatyon düzeyinde azalmaya yol açtığı belirlenmiştir. Buna karşın, östrojen uygulaması menopozda yapılan egzersiz nedeniy-le karaciğerde oluşan oksidan stresi engellemiştir. Egzer-sizle veya egzersize östrojen tedavisinin eklenmesiyle böbrek fonksiyonları önemli ölçüde etkilenmezken, kemik yapısında tek başına östrojene kıyasla daha olumlu deği-şiklikler gözlenmiştir.Sonuç: Östrojen replasmanı kemik dokusundaki olum-lu etkilerinin yanı sıra karaciğer ve böbrekte oksidan stresi azaltmakta ve özellikle karaciğerde egzersize bağlı gelişen oksidan stresi baskılayarak koruyucu etki göstermektedir.
  • PublicationOpen Access
    Myrtus communis L. Extract Ameliorates High Fat Diet Induced Kidney and Bladder Damage by Inhibiting Oxidative Stress and Inflammation
    (2022-12-02) ERTAŞ, BÜŞRA; ŞEN, ALİ; AKAKIN, DİLEK; ERCAN, FERİHA; Kanpalta Mustafaoğlu F., Ertaş B., Şen A., Akakın D., Şener G., Ercan F.
    Objective: Obesity is associated with many diseases, including urinary system disorders such as chronic kidney disease and overactive bladder syndrome. Myrtus communis L. (MC) extract has been reported to have antioxidant and anti-inflammatory effects. The aim of this study was to investigate the protective effects of MC extract on high-fat diet (HFD)-induced kidney and bladder damage. Materials and Methods: Wistar albino male rats were divided into three experimental groups: control, HFD and HFD+MC. Experimental groups were fed a standard diet (control group) or HFD (HFD and HFD+MC groups) for 16 weeks. MC extract (100 mg/kg) was administered to the HFD+MC group orally during the last 4 weeks (5 days/week) of the experiment. Highdensity lipoprotein, total cholesterol, triglyceride and leptin levels were measured in blood serum. Tissue malondialdehyde (MDA), glutathione (GSH), 8-hydroxy-2'-deoxyguanosine (8-OHdG) and myeloperoxidase (MPO) levels were evaluated biochemically. Kidney and bladder morphology, NADPH oxidase-2 (NOX-2) and nuclear factor-kappa B (NF-ҡB)-positive and apoptotic cells were evaluated histologically. Results: Lipid profiles altered and leptin levels increased in blood serum. MDA, 8-OHdG and MPO levels increased and GSH level decreased in kidney and bladder in the HFD group. Moreover, degenerated kidney and bladder morphology, increased NOX-2 and NF-ҡB-positive and apoptotic cells were observed in this group. All of these biochemical and histological parameters were ameliorated in the HFD+MC group. Conclusion: HFD-induced obesity causes kidney and bladder damage by oxidative and inflammatory processes. MC extract may reduce oxidative stress and inflammation and play a protective role in obesity-related kidney and bladder damage.
  • PublicationOpen Access
    Neuropeptide W Exhibits Preventive and Therapeutic Effects on Acetic Acid-Induced Colitis via Modulation of the Cyclooxygenase Enzyme System
    (2023-01-01) ARABACI TAMER, SEVİL; ERCAN, FERİHA; YEGEN, BERRAK; ARABACI TAMER S., Akbulut S., Erdogan O., Cevik O., ERCAN F., YEGEN B.
    Background The novel peptide neuropeptide W (NPW) was originally shown to function in the control of feeding behavior and energy homeostasis. The aim of this study was to elucidate the putative preventive and therapeutic effects of NPW on colitis-associated oxidative injury and the underlying mechanisms for its action.Methods Sprague-Dawley rats in the acute colitis groups received NPW (0.5, 1 or 5 mu g/kg/day) injections prior to induction of colitis with acetic acid, while the chronic colitis groups were treated after the induction of colitis. In both acute and chronic colitis (CC) groups, treatments were continued for 5 days and the rats were decapitated at the 24th hour of the last injections and colon tissues were collected for assessments.Results NPW pretreatment given for 5 days before colitis induction, as well as treating rats with NPW during the 5-day course of CC, abolished colonic lipid peroxidation. NPW treatment prevented colitis-induced reduction in blood flow, diminished neutrophil infiltration, and pro-inflammatory cytokine responses. NPW pretreatment only at the higher dose reduced colonic edema and microscopic score and preserved colonic glutathione stores. Elevations in cyclooxygenase (COX) enzyme activity and COX-1 protein level during the acute phase of colitis as well as reduction in COX-2 were all reversed with NPW pretreatment. In contrast, NPW treatment was effective in reducing the elevated COX-2 concentration during the chronic phase.Conclusions NPW alleviates acetic acid-induced oxidative colonic injury in rats through the upregulation of colonic blood flow as well as the inhibition of COX-2 protein expression and pro-inflammatory cytokine production.
  • PublicationOpen Access
    Morphological and biochemical investigation of the protective effects of panax ginseng on methotrexate-induced testicular damage
    (2023-06-01) AKBAY, TUĞBA; ERCAN, FERİHA; Karakaya F. B., Macit Ç., Sivas G. G., Akbay T., Şeber G., Ercan F.
    Objective: Methotrexate (MTX) is a chemotherapeutic agent that causes testicular toxicity used in the cure of various types ofcancer. The anti-oxidant and anti-cancer effects of Panax ginseng (PxG) have been reported in both experimental and clinical studies. This study aims to examine the healing effect of PxG on testicular damage induced by MTX.Materials and Methods: Sprague Dawley male rats (8-week-olds) were used in the study. A single dose ofMTXdissolved in saline(20 mg/kg) was given to MTX and MTX+PxG groups by intraperitoneal injection. PxG dissolved in saline (100 mg/kg) was given by orogastric gavage once a day for 5 days to the MTX+PxG group. Saline was given to the control and MTX groups orally during the experiments. After decapitation, the testis sampleswere obtained. Seminiferous tubules and basement membranewere evaluated histopathologically. Seminiferous tubule diameter and germinal epithelium thickness were measured. Furthermore, oxidative stress parameters such as malondialdehyde, glutathione, superoxide dismutase, and glutathione-S-transferase were measured.Results: MTX treatment caused seminiferous tubule degeneration with a decrease in Johnsen’s score, the seminiferous tubule’sdiameter, and the germinal epithelium’s thickness. Parallel with the histopathological results increased testicular oxidative stress with an increase in malondialdehyde level and a decrease of endogenous anti-oxidant activity with a decrease in glutathione level and glutathione-S-transferase and superoxide dismutase activities. PxG treatment improved these histological and biochemical parameters in MTX-induced testis cytotoxicity.Conclusion: MTX treatment causes testicular damage via the oxidative processes. PxG treatment ameliorates MTX-inducedtesticular damage by inhibiting oxidative stress.
  • PublicationOpen Access
    The alterations of blood-testis barrier in experimental testicular ınjury models
    (2022-05-01) ERCAN, FERİHA; Ercan F., Acıkel Elmas M.
    The blood-testis barrier is found between the Sertoli cells and divides the seminiferous tubule epithelium into basal and adluminal compartments. The germinal cell renewal, differentiation and cell cycle progression up to the preleptotene spermotocytes stage take place in the basal compartment, however, meiosis, spermiogenesis and spermiation take place in the adluminal compertment. The blood-testis barrier consists of tight junctions as well as ectoplasmic specialisations, desmosomes and gap junctions to create specific microenvironment for the completion of spermatogenesis to form spermatozoa. The blood-testis barrier is not a static ultrastructure, it undergoes extensive restructuring during the seminiferous tubule epithelial cycle of spermatogenesis to allow the transit of preleptotene spermotocytes at the blood-testis barrier from basal compartment towards the adluminal compartment. The functions of the blood-testis barrier include preventing the transport of biomolecules into the paracellular space, forming an immunological barrier, separating cellular processes during the spermatogenic epithelial cycle, and establishing the cellular polarity of the seminiferous tubule. However, various environmental conditions, chemotherapeutic agents, toxic substances and lifestyle have degenerative effects on blood-testis barrier, resulting in testicular damage, altered sperm parameters and ultimately male infertility. The alterations in morphological and molecular organization of blood-testis barrier in different experimentally induced testis injury models arc reviewed in this article.
  • PublicationOpen Access
    Melatonin alleviates ovariectomy-induced cardiovascular inflammation in sedentary or exercised rats by upregulating SIRT1
    (2022-12-01) ERCAN, FERİHA; YILDIRIM, ALPER; YEGEN, BERRAK; Arabacı Tamer S., Altınoluk T., Emran M., Korkmaz S., Yüksel R. G., Baykal Z., Dur Z. S., Levent H. N., Ural M. A., Yüksel M., et al.
    © 2022, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.We aimed to evaluate the impact of hormone replacement, melatonin, or exercise alone or their combination on oxidative damage and functional status of heart, brain, and aorta of ovariectomized (OVX) rats and to determine whether the signaling pathway is dependent on sirtuin-1 (SIRT1). Ovariectomized Sprague Dawley rats were orally given either a hormone replacement therapy (1 mg/kg/day,17β estradiol; HRT) or melatonin (4 mg/kg/day) or HRT + melatonin treatments or tap water, while each group was further divided into sedentary and exercise (30 min/5 days/week) groups. After the heart rate measurements and memory tests were performed, trunk blood was collected at the end of the 10th week to determine metabolic parameters in serum samples. Tissue samples of abdominal aorta, heart, and brain were taken for biochemical measurements and histopathological evaluation. Heart rates and memory performances of the OVX rats were not changed significantly by none of the applications. Melatonin treatment or its co-administration with HRT upregulated the expressions of IL-10 and SIRT1, reduced the expressions of IL-6 and TNF-α, and reduced DNA damage in the hearts and thoracic aortae of non-exercised rats. Co-administration of melatonin and HRT to exercised OVX rats reduced inflammatory response and upregulated SIRT1 expression in the aortic and cardiac tissues. The present study suggests that melatonin treatment, either alone or in combination with exercise and/or HRT, upregulates SIRT1 expression and alleviates oxidative injury and inflammation in the hearts and aortas of OVX rats. Melatonin should be considered in alleviating cardiovascular disease risk in postmenopausal women.
  • PublicationOpen 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.
  • PublicationOpen Access
    Evaluation of toxic effects of dapagliflozin on reproductive system in diabetic rats
    (2022-01-01) ERCAN, FERİHA; Karaca B. U. , Boran T., Koroglu A. K. , ERCAN F., Ozhan G.
    Background/aim: Dapagliflozin (DAPA), sodium-glucose cotransporter 2 (SGLT2) inhibitor, is an insulin-independent antidiabetic drug used to control hyperglycaemia by promoting glucose excretion from the kidney. Its adverse effects include orthostatic hypotension, dehydration and urinary tract and genital infections caused by glycosuria. DAPA is subjected to constant additional monitoring, as drug-related adverse reactions are frequently updated in line with the results of case studies, clinical trials and in vivo studies. Some antidiabetic drugs have shown potential harmful effects on the male reproductive system; however, the effects of DAPA have not been sufficiently studied in this capacity. Aiming to fill this gap in the literature, the present work investigates the toxic effects of DAPA on the male reproductive system.
  • PublicationOpen Access
    Exercise improves testicular morphology and oxidative stress parameters in rats with testicular damage induced by a high-fat diet
    (2022-09-01) BİNGÖL ÖZAKPINAR, ÖZLEM; ERCAN, FERİHA; Açıkel Elmas M., Bingöl Özakpınar Ö., Şner G., Arbak S., Ercan F.
  • PublicationOpen Access
    Gastroprotective effect of vanillic acid against ethanol-induced gastric injury in rats: involvement of the NF-κB signalling and anti-apoptosis role
    (2024-12-01) ERCAN, FERİHA; Arabacı Tamer S., Eskiler G. G., ERCAN F.
    Background: Vanillic acid (VA; 4-hydroxy-3-methoxybenzoic acid) is a flavouring agent found in various natural sources such as olives, fruits, and green tea. While VA exhibits numerous pharmacological effects, its potential protective effects against gastric injury warrants further investigation. Therefore, the primary objective of this study is to elucidate investigate the gastroprotective properties of VA against ethanol-induced gastric injury. Methods and results: Rats were orally administered either saline or VA at different doses (50, 100, and 200 mg/kg/day), with omeprazole (20 mg/kg) serving as a positive control, for fourteen consecutive days before ethanol administration. Blood and gastric tissue samples were collected one hour after ethanol administration for biochemical, molecular, and histological analyses. Pre-treatment with VA before ulcer induction alleviated both macroscopic and microscopic damage. It also increased antioxidant glutathione levels and decreased malondialdehyde and myeloperoxidase activity, along with reducing inflammatory markers such as tumour necrosis factor (TNF)-α, interleukin (IL)-6, and nuclear factor kappa B (NF-κB). Additionally, VA pre-treatment reversed the elevation of Bax mRNA expression and gastric caspase-3 levels induced by gastric damage. It also mitigated the reduction in Bcl-2 mRNA expression. Conclusion: These findings suggest that VA exerts protective effects against ethanol-induced gastric injury in rats. It achieves this by augmenting gastric antioxidant capacity and mitigating oxidative, inflammatory, and apoptotic damage.