Person: ERCAN, FERİHA
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ERCAN
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FERİHA
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Publication Open 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.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 Open Access Apocynin exhibits an ameliorative effect on endothelial dysfunction/atherosclerosis-related factors in high-fat diet-induced obesity in rats(2024-05-31) ERTAŞ, BÜŞRA; KOÇYİĞİT SEVİNÇ, SEVGİ; ERCAN, FERİHA; ORUN, OYA; AKKİPRİK, MUSTAFA; ÇETİNEL, ŞULE; Bulbul Ayci N., ERTAŞ B., Keles Kaya R., Kocyigit Sevinc S., Amuran G. G., ERCAN F., Sener G., ORUN O., AKKİPRİK M., ÇETİNEL Ş.Objective: The aim of this study was to reveal the effect of apocynin (APO) on the factors involved in obesity-related endothelial dysfunction (ED) and atherosclerosis (AS). Materials and Methods: Male Wistar albino rats were divided into control (CNT), high-fat diet (HFD) and HFD+APO groups. HFD and HFD+APO groups were fed HFD for sixteen weeks. APO (25 mg/kg) was administered to the HFD+APO group for the last four weeks. The effects of APO on: AS-related metabolic parameters (triglyceride, total cholesterol, high-density lipoprotein-cholesterol, insulin and leptin), oxidative stress (OS), [ malondialdehyde, glutathione, nicotinamide adenine dinucleotide phosphate (NADPH)-oxidase-2, oxidised-low-density lipoprotein (ox-LDL) and 8-hydroxy-2-deoxyguanosine], low-density lipoprotein and ox-LDL uptake potential (activin receptor-like kinase-1 and lectin-like oxidized low-density lipoprotein receptor-1, respectively), tissue inflammation (myeloperoxidase, monocyte-chemoattractant-protein-1, tumor necrosis factor-alpha), ED (endothelial-nitric oxide synthase, inducible-nitric oxide synthase, nitric oxide), programmed cell death (terminal deoxynucleotidyl-transferase-dUTP-nick-end labeling, cleaved-poly-ADP-ribose-polymerase, gasdermin-D N-terminal fragment, caspase-1), smooth muscle cell transformation (alpha-smooth muscle actin), histology and ultrastructure of thoracic aorta were evaluated. Results: In obesity, APO had an ameliorative effect on metabolic parameters, OS, inflammation, ED, programmed cell death and oxLDL uptake potential, but not on foam cell formation and LDL uptake potential. Conclusion: Apocynin may improve ED and AS in obesity by suppressing OS-linked factors involved in the early stage of AS.