WoS İndeksli Yayınlar Koleksiyonu
Permanent URI for this collectionhttps://hdl.handle.net/20.500.14627/6
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Article Lactobacillus Rhamnosus GG Alleviates Bisphenol-A Induced Oxidative Stress in Serum(Marmara University, Faculty of Pharmacy, 2025) Şener, Göksel; Tunali-Akbay, Tugba; Dorucu, Dogancan; Ede-Pazarbasi, Seren; Dede, Pınar; Ede-Pazarbas, SerenThe objective of this investigation was to identify changes in the serum oxidant-antioxidant balance of rats exposed to bisphenol A (BPA) and to investigate the impact of Lactobacillus rhamnosus GG (LGG) administration on those changes. Twenty-four rats (Wistar Albino, 250-300 grams, male) were divided into control, BPA, and BPA+LGG groups with an equal number of rats. BPA and LGG were applied to the rats in the relevant groups for six weeks, five days each week. Six weeks later, the blood samples were withdrawn and serum samples were prepared. Total oxidant and antioxidant status (TAS), glutathione, and lipid peroxidation determinations were determined in serum samples, and the oxidative stress index was calculated. BPA exposure decreased serum total antioxidant status and increased serum total oxidative status, oxidative stress index, and lipid peroxidation level compared to the control group. LGG administration improved the increased serum oxidative stress caused by BPA. Administration of LGG to BPA-treated rats reversed oxidative stress-induced changes. In conclusion, administration of Lactobacillus rhamnosus GG to rats for 30 consecutive days prevented oxidative stress in serum caused by bisphenol A.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 The Effects Of<i> Panax</I><i> Ginseng</I> on Serum Oxidative Stress Following Bisphenol a Exposure(Istanbul Univ, 2024) Fazalyar, Najiullah; Pazarbasi, Seren Ede; Dorucu, Dogancan; Sener, Goksel; Tunali-Akbay, Tugba; Ede-pazarbasi, SerenObjective: Bisphenol A (BPA) is a toxic compound that causes oxidative stress by disrupting antioxidant enzymes and promoting tissue lipid peroxidation. This study aimed to examine the impacts of BPA on serum oxidative stress in rats and to detect the antioxidant feature of Panax ginseng (PxG) in reducing BPA-induced oxidative stress. Materials and Methods: Wistar Albino rats (250-300 g) were divided into control, control + PxG, BPA, and BPA + PxG groups. 50 mg/kg BPA and 100 mg/g PxG were given for six weeks. Serum total antioxidant and oxidant status, lipid peroxidation, and glutathione levels were determined. Results: BPA administration increased total oxidant status and lipid peroxidation, while PxG administration to the BPA group decreased these parameters. PxG also increased total antioxidant status and glutathione levels compared to the BPA group. Conclusion: BPA was seen to cause an increase in oxidative parameters and PxG administration to restore the oxidative stress that was generated after BPA exposure, suggesting that this may help to prevent the adverse effects caused by BPA exposure.Article Citation - WoS: 1Citation - Scopus: 2The Effect of Whey Proteins on the Brain and Small Intestine Nitric Oxide Levels: Protein Profiles in Methotrexate-Induced Oxidative Stress(Istanbul Univ, 2022) Yilmaz, Sumeyye; Tufan, Elif; Sivas, Guzin Goksun; Gokmen, Begum Gurel; Dursun, Ercan; Ozbeyli, Dilek; Tunali-Akbay, Tugba; Şener, Göksel; Karaoğlu, Sümeyye YılmazObjectives: The aim of this study was to determine the effects of whey proteins on methotrexate (MTX)-induced brain and small intestine damage. Materials and Methods: 30 Sprague Dawley rats (200-300 g) were divided into four groups: Control, control + whey, MTX, and MTX+whey. MTX was administered at 20 mg/kg (single dose) intraperitoneally to the MTX group rats, and 2 mg/kg of whey protein were administered by oral gavage for 10 days to the whey groups. Lipid peroxidation, glutathione, and nitric oxide (NO) levels, as well as glutathione-Stransferase and superoxide dismutase activities were measured in the brain and small intestine. SDS-polyacrylamide gel electrophoresis of the brain and intestine tissues were also carried out. Results: While MTX treatment caused oxidative damage in the brain and small intestine, whey protein administration ameliorated MTXinduced oxidative stress. MTX administration did not change the brain's NO level, while an increase in intestinal NO level was detected. Conclusion: MTX induced oxidative stress in the brain and small intestine changed the protein metabolism in these tissues regardless of reduced food intake. Consecutive 10-day administration of whey proteins has shown its therapeutic effect on MTX-induced brain and small intestine oxidative damage.Article Brain in Metabolic Syndrome Model: the Effect of Exercises and Caloric Restriction(Marmara Univ, 2022) Alev-Tuzuner, Burcin; Genc-Kahraman, Nevin; Ipekci, Hazal; Ustundag, Unsal Veli; Tunali-Akbay, Tugba; Emekli-Alturfan, Ebru; Yarat, Aysen; Alturfan, Ebru Emeklı; Akbay, Tugba TunalıCaloric restriction (CR) and exercise (EX) have impacts on improving metabolic risk factors. This study aimed to investigate the changes in the brain after EX and/or CR in metabolic syndrome (MeS) induced by a high fructose diet in rats. Sprague-Dawley male rats were divided into five groups. Drinking water including 10% fructose solution was given to rats for 12 weeks to develop a MeS rat model. Animals with MeS were submitted to EX and/or CR for 6 weeks. Blood glucose, and brain tissue damage and antioxidant parameters were measured. Brain lipid peroxidation, sialic acid, mucin, fucose levels increased in the MeS group compared to the control (C) group. These parameters reduced significantly in the metabolic syndrome with caloric restriction (MeS+CR) group, and more significantly in the metabolic syndrome with exercise and caloric restriction group (MeS+EXCR), compared to the MeS group. Glutathione levels, superoxide dismutase and catalase activities decreased in the MeS group compared to the C group, increased both in the MeS+CR group, and MeS+EXCR group compared to the MeS group. High fructose diet consumption can lead to brain tissue damage and decreased antioxidant levels were found to be improved best in the MeS+EXCR group.Article Citation - WoS: 6Citation - Scopus: 6Myrtle Improves Renovascular Hypertension-Induced Oxidative Damage in Heart, Kidney, and Aortic Tissue(Springer, 2022) Arslan, Sule; Ozcan, Ozan; Gurel-Gokmen, Begum; Cevikelli-Yakut, Zatiye Ayca; Saygi, Halil Ibrahim; Sen, Ali; Tunali-Akbay, TugbaRenovascular hypertension is defined as the reduction in renal perfusion resulting in sustained hypertension. This study aims to investigate the possible effects of myrtle leaf extract (Myrtus communis L.) on, heart, kidney and aorta tissues in the experimental renovascular hypertension (RVH). 32 male Wistar Albino rats were divided into four groups as control, hypertension, hypertension+ramipril, and hypertension+myrtle leaf extract treatment groups. RVH model was induced by Goldblatt's 2-kidney 1-clip method. 12 weeks later than the treatment blood pressures were recorded and oxidant and antioxidant parameters, tissue factor activity, and histological analysis were determined in the kidney, heart, and aortic tissues. The blood pressure levels of the hypertension group significantly increased compared to the control group. Administration of myrtle leaf extract and ramipril significantly decreased the increased blood pressure. In the hypertension group, oxidative damage increased in the kidney, heart, and aorta tissues. In the histological evaluation of tissues in RVH, heart muscle fibres degenerated. Bowman capsule and glomeruli dilated and tubules damaged in the kidney. Myrtle leaf extract administration regenerated the damages and degenerations. The administration of myrtle leaf extract restored the impaired oxidant-antioxidant balance in the heart, kidney and aorta tissues of hypertensive rats. Myrtle leaf extract can be considered as an alternative antihypertensive treatment target in the prevention of oxidative stress-induced damage in renovascular hypertension.
