WoS İndeksli Yayınlar Koleksiyonu
Permanent URI for this collectionhttps://hdl.handle.net/20.500.14627/6
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Article Unraveling the Persistent Renal Impact of Intrauterine Growth Restriction and Catch-Up Growth: Integrating Morphological Insights with Metabolomic Profiling(Springer, 2025) Esrefoglu, Mukaddes; Koktasoglu, Fatmanur; Bayindir, Nihan; Cimen, Fatma Bedia Karakaya; Kirmizikan, Seda; Hekimoglu, Emine Rumeysa; Selek, SahabettinThe study aimed to investigate the long-term effects of IUGR and consequent catch-up growth on metabolic health by using a comprehensive approach that included histopathological, immunohistochemical, biochemical, and metabolomics analyses. Sprague-Dawley pregnant rats either undergo bilateral uterine artery ligation or a sham surgery on the 19th day of gestation. The offspring reached catch-up growth, kidney samples were collected at postnatal weeks 2, 4, and 8 for analysis. IUGR rats exhibited a spectrum of changes including reduced glomeruli number, proliferating cell number, altered oxidative stress markers, various enzymes involved in Krebs cycle, mitochondrial dynamics, and energy metabolism. Examination of the 8-week-old cohort identified a broader spectrum of metabolic alterations, notably in the biosynthesis of phenylalanine, tyrosine, and tryptophan, phenylalanine, tyrosine, glyoxylate, dicarboxylate, pyruvate, alanine, aspartate, and glutamate metabolism, glycolysis/gluconeogenesis and citrate (TCA) cycle. Our metabolomics analysis provides insights into the potential disease susceptibility of individuals born with IUGR, including obesity, diabetes, hypertriglyceridemia, cardiovascular diseases, and mental retardation. These findings underscore the intricate interplay between intrauterine conditions and long-term metabolic health outcomes, highlighting the need for further investigation into preventive and therapeutic strategies to mitigate the risk of metabolic diseases in individuals with a history of IUGR.Article NADPH Oxidase-2 Inhibitor Apocynin Attenuates High-Fat Diet-Induced Kidney and Bladder Injury(Marmara Univ, Fac Medicine, 2025) Kanpalta Mustafaoglu, Fatma; Ertas, Busra; Sener, Goksel; Ercan, FerihaObjective: This study aimed to evaluate the effects of NADPH oxidase-2 (NOX-2) inhibitor apocynin (APC) on high-fat diet (HFD)induced renal and bladder injury. Materials and Methods: Wistar albino rats were divided into 4 groups: Control, HFD, HFD+dimetyl sulfoxide (DMSO), and HFD+APC. Rats in HFD, HFD+DMSO, and HFD+APC groups were fed with HFD for sixteen weeks. In the last 4 weeks of the experiment, either DMSO or APC (25 mg/kg, dissolved in DMSO) was applied to the HFD+DMSO or HFD+APC groups. Lipid profiles and leptin values were measured in blood serum. Renal and bladder oxidant/antioxidant parameters, histological changes in the tissues, NOX-2-, nuclear factor kappa B (NF-& kgreen;B)-immunopositive and apoptotic cells were evaluated. Results: At the end of the experiment, leptin, cholesterol, and triglyceride levels were higher and high-density lipoprotein levels were lower in the HFD and HFD+DMSO groups compared to controls. In these experimental groups, an increase in malondialdehyde, 8-hydroxy-deoxyguanosine and myeloperoxidase levels and a decrease in glutathione levels, as well as an increase in collagen, NOX-2-and NF & kgreen;-B-immunopositive and apoptotic cells were found. Also, a deterioration in kidney and bladder morphology was observed. All these biochemical and histopathological findings improved in the HFD+APC group. Conclusion: High-fed diet causes renal and bladder injury by increasing NOX-2 activity and inflammation via oxidative stress. APC might alleviate tissue injury by inhibiting oxidative stress.Article Panax Ginseng Extract Ameliorates Methotrexate-Induced Multi-Organ Damage Via the Regulation of Oxidative Stress(Marmara Univ, 2023) Macit, Caglar; Ede-Pazarbasi, Seren; Yilmaz-karaoglu, Suemeyye; Tunali-Akbay, Tugba; Karakaya-Cimen, Fatma Bedia; Ercan, Feriha; Sener, Goksel; Akbay, Tugba Tunalı-Oxidative damage plays an important role in organ toxicities caused by methotrexate (MTX). This study aimed to determine the antioxidant effects of Panax ginseng (PxG) extract against MTX-induced liver, lung, ileum and kidney damage. Twenty-four Sprague Dawley male rats (weight 250-300 g) were used in the study. The animals were randomly separated into three groups: a) Control, b) MTX-treated (MTX) and c) MTX+PxG-treated (MTX+PxG) groups. MTX was administered intraperitoneally at 20 mg/kg, as a single dose to MTX and MTX+PxG groups. PxG was administered orally at 100 mg/kg to the MTX+PxG group for five days. Saline was given to the control and MTX groups for 5 days. At the end of the experiment, liver, lung, ileum, and kidney samples were obtained. Malondialdehyde (MDA) and glutathione (GSH) levels, superoxide dismutase (SOD), glutathione-S-transferase (GST) and tissue factor (TF) activities were determined in all tissues. In addition, histological examinations were done through light microscopy. GraphPad Prism 5v. was used for statistics, and p<0.05 were considered significant. Administration of MTX caused severe injury in tissues. Findings showed that MDA level, SOD, and GST activities were significantly normalized in the MTX+PxG group compared to the control group. A significant reduction in GSH level observed in the MTX group was reversed with PxG administration In addition, TF activity and total protein levels were found to be impaired in the MTX group, but TF activity was significantly improved in liver and lung tissues and total protein level was significantly reversed in lung and ileum in MTX+PxG group. The results of histological examinations showed that MTX-induced damage was ameliorated with the PxG administration. In conclusion, this study shows that Panax ginseng, thanks to its antioxidant properties, reversed MTX-induced tissue damage and therefore may be beneficial against side effects in patients undergoing chemotherapy.Article Citation - Scopus: 1Protective Effects of <i>momordica Charantia</I> (bitter Melon) Against Methotrexate-Induced Kidney Damage(Bentham Science Publ Ltd, 2023) Macit, Caglar; Ozbeyli, Dilek; Cevik, Ozge; Cetin, Melisa; Sener, Goksel; Ozkan, SevilBackground Methotrexate is a cytotoxic chemotherapeutic agent that has severe side effects, such as nephrotoxicity. Momordica charantia is a bright yellow-orange fruity plant that has been shown to have antioxidant, antidiabetic, and anti-inflammatory properties. Objective This study scrutinized the protective effects of Momordica charantia extract against methotrexate-induced nephrotoxicity. Methods 24 Sprague Dawley male rats were divided into three experimental groups (8 rats in each): Control (C); Methotrexate (MTX); and Methotrexate plus Momordica charantia (MTX+MC). All rats were fed ad libitum and tap water. Methotrexate was administered at 20 mg/kg intraperitoneally as a single dose. In the MTX+MC group, MC was administered at a dose of 50mg/kg for 5 days orally. At the end of the 5th day, the rats were decapitated and kidney samples were taken to analyze glutathione (GSH), malondialdehyde (MDA), myeloperoxidase (MPO), 8-hydroxy-2'-deoxyguanosine (8-OHdG) and caspase-3 activity. Data was analyzed with GraphPad Prism 5.0. Results Findings showed that while there was a significant increase in MDA, MPO, 8-OHdG levels, and an essential reduction in GSH levels in the MTX-treated group when compared with the control group, bitter melon treatment significantly reversed MDA, MPO, and 8-OHdG levels (p< 0.001). GSH level elevation was observed in the MTX-MC group when compared to the MTX-treated group (p< 0.001). Conclusion This study showed that bitter melon is thought to have a protective effect against kidney damage caused by methotrexate. With future studies, we believe that the use of bitter melon extract as a protective agent in kidney damage caused by drug-induced oxidative damage will bring an innovative approach to treatment.Article Citation - WoS: 4Citation - Scopus: 4Whey Protein Concentrate Ameliorates the Methotrexate-Induced Liver and Kidney Damage(Cambridge Univ Press, 2023) Tufan, Elif; Sivas, Guezin Goksun; Gurel-Gokmen, Begum; Yilmaz-Karaoglu, Suemeyye; Dursun, Ercan; Caliskan-Ak, Esin; Tunali-Akbay, Tugba; Yllmaz-Karaoǧlu, SÜmeyye; Çallşkan-Ak, EsinMethotrexate (MTX) is a cytotoxic immunosuppressant that is widely used in the treatment of tumours, rheumatoid arthritis and psoriasis. This study aims to evaluate the effects of whey proteins on MTX-induced liver and kidney damage by focusing on oxidant-antioxidant systems and eating habits. The study was conducted in four groups of thirty Sprague-Dawley rats (control, control + whey protein concentrate (WPC), MTX, MTX + WPC). A single dose of 20 mg/kg MTX was administered intraperitoneally to the MTX groups. Control and MTX groups were given 2 g/kg WPC by oral gavage every day for 10 d. At the end of day 10, blood samples were drawn and liver and kidney tissues were removed. MTX administration increased the lipid peroxidation level and decreased glutathione level, superoxide dismutase and glutathione-S-transferase activities in the liver and kidney. Administration of WPC significantly reduced the damage caused by MTX in the liver and kidney. While a decrease in serum urea level and an increase in serum creatinine level were detected in the MTX group, WPC administration reversed these results up to control group levels. Administration of WPC to the MTX group significantly reversed the histopathological damage scores of the liver and kidney. WPC administration ameliorated the MTX-induced oxidative damage in the liver and kidney tissues due to its antioxidant properties. Liver and kidney damage can be prevented by using whey proteins as a nutraceutical in MTX therapy. In conclusion, whey proteins demonstrated a protective effect against MTX-induced liver and kidney damage.Article Citation - WoS: 3Morphological and Biochemical Investigation of the Healing Effects of Exercise on High Fat Diet Induced Kidney and Bladder Damage(Marmara Univ, inst Health Sciences, 2022) Elmas, Merve Acikel; Ozakpinar, Ozlem Bingol; Kolgazi, Meltem; Sener, Goksel; Ercan, FerihaObjective: The aim of this study was to evaluate the ameliorative effects of swimming training on renal and bladder damage caused by a highfat diet (HFD) using morphological and biochemical measurements. Methods: Sprague Dawley rats were fed either standard chow (CONT, 6% fat) or HFD (45% fat) for 18 weeks, these rats were divided into two subgroups at the last 6 weeks of the experiment. The exercise groups (CONT+EXC, HFD+EXC) were trained daily swimming sessions (1 h per day for 5 days/week) during the last 6 weeks. Kidney and bladder samples were prepared for light and electron microscopic examination at the end of experiment. Malondialdehyde, glutathione, interleukin-6, and tumor necrosis factor-a were measured by biochemically. Results: Regular morphology of the renal cortex and bladder mucosa was observed in the CONT and CONT +EXC groups. Degenerated renal corpuscles and proximal tubules in the kidney and degenerated urothelium with leaky tight junctions and mast cell increase in the bladder mucosa were observed in the HFD group. Ameliorated renal cortex and bladder mucosa were observed in the HFD+EXC group. In addition, malondialdehyde, glutathione, interleukin-6, and tumor necrosis factor-a levels were also consistent with the histological findings. Conclusion: HFD-induced renal and bladder damage may be related to increased oxidative damage. It was observed that the histological damage and altered oxidative stress parameters could be reversed by swimming training, and it is thought that moderate swimming exercise may play a role in regulating oxidative stress.