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    Ameliorative effects of thymoquinone on the caspase 3, kidney function and oxidative stress tartrazine-induced nephrotoxicity
    (Pergamon-Elsevier Science Ltd, 2024) Erdemli, Zeynep; Gul, Mehmet; Gokturk, Nurcan; Kayhan, Elif; Demircigil, Nursena; Ozsoy, Eda Nur; Bag, Harika Gozukara
    First in the literature this study aimed to investigate the effects of Tartrazine, a common industrial food dye, on kidney and whether Thymoquinone has a protective effect in tartrazine-induced nephrotoxicity. The study conducted on the rats bred at I(center dot)non & uuml; University Experimental Animals Production and Research Center. Wistar albino rats were randomly divided into 4 groups, where each group included 8 rats: control, Tartrazine, Thymoquinone, and Tartrazine + Thymoquinone groups. The experiments continued for 3 weeks and then, kidney tissues and blood samples were collected from the rats under anesthesia. Malondialdehyde (MDA), super oxidized dismutase (SOD), total oxidant status (TOS), increase in Oxidative stress index (OSI), glutathione (GSH), Glutathione peroxidase (GSH-Px), catalase (CAT), Total antioxidant status (TAS) levels decreased in the kidney tissues collected from the tartrazine group. Serum Bun and Creatinine levels increased in the tartrazine group. Tartrazine administration damaged and degenerated the glomeruli and cortical distal tubes in the histopathology of kidney tissues, also different degrees of inflammatory cell infiltration were observed in the renal cortex and medulla. Thymoquinone and tartrazine administration improved both biochemical and histopathological parameters. Tartrazine administration induced nephrotoxicity. This could be observed with the increase in oxidant capacity and the deterioration of kidney functions. Thymoquinone was observed to demonstrate strong antioxidant properties. Thymoquinone could be used primarily as a protective agent against Tartrazine-induced toxicity.
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    Ninety Sixth-Hour Impact of Scalding Burns on End Organ Damage, Systemic Oxidative Stress, and Wound Healing in Rats Treated With Three Different Types of Dressings
    (Oxford Univ Press, 2024) Aslan, Mehmet; Gul, Mehmet; Uremis, Nuray; Akbulut, Sami; Gurunluoglu, Semra; Ozsoy, Eda Nur; Turkoz, Yusuf
    In this study, we investigated the effects of 3 different burn dressing treatments, including experimental, silver, and modern dressing materials, on systemic oxidative stress in rats with severe scald burns within the first 96 h. The rats were divided into five groups: a burn group (n = 10), a polylactic membrane group (n = 10), a silver sulfadiazine group (n = 10), a curcumin group (n = 10), and a control group (n = 10), consisting of equal numbers of female and male rats. In the first 4 groups, 30% of the rats' total body surface area was scalded at 95 degrees C. The burn group was not treated. Each group was treated with group-name dressing material. The control group was neither treated nor burned. The rats were sacrificed, and blood and tissue samples were obtained at the 96th hour when severe effects of oxidative stress developed postburns. Systemic inflammatory biomarkers and oxidative stress parameters were examined. In addition, apoptosis and organ damage in liver, kidney, lung, and skin tissues were evaluated biochemically and histopathologically. When the parameters were statistically analyzed, we found that the systemic levels of oxidative stress and inflammatory damage to liver, kidney, and lung tissues were lower in the 3 treated groups than in the burn group. We believe that the dressing material's efficacy in the treatment of severe burns may be dependent on its ability to combat oxidative stress and inflammation.
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    Protective effects of vitamin E against acrylamide-induced hepatotoxicity and nephrotoxicity from fetal development to adulthood: Insights into Akt/ NF-?B and Bcl-xL/Bax signaling pathways
    (Elsevier Ireland Ltd, 2024) Uremi, Nuray; Uremi, Muhammed Mehdi; Gul, Mehmet; Ozsoy, Eda Nur; Turkoz, Yusuf
    Acrylamide (ACR), a toxin present in fried and baked carbohydrate-rich foods, is known to cause liver and kidney damage. This study aimed to investigate the mechanisms of oxidative stress, inflammation, and apoptosis that contribute to liver and kidney damage induced by chronic administration of ACR. Additionally, the effectiveness of vitamin E in mitigating these toxic effects was examined. The study initially involved dividing 40 pregnant rats into four groups. After lactation, the research continued with male offspring rats from each group. The offspring rats were divided into Control, Vitamin E, ACR, and ACR + Vitamin E groups. Following ACR administration, liver and kidney function tests were performed on serum samples. Biochemical analyses, evaluation of inflammation markers, histopathological examination, and assessment of protein levels of Akt/I kappa B alpha/NF-kappa B, Bax, Bcl-xL, and Caspase-9 were conducted on liver and kidney tissues. The analysis demonstrated that ACR adversely affected liver and kidney function, resulting in oxidative stress, increased inflammation, and elevated apoptotic markers. Conversely, administration of vitamin E positively impacted these parameters, restoring them to control levels. Based on the results, the mechanism of ACR's action on oxidative stress and inflammation-induced liver and kidney damage may be associated with the activation of apoptotic markers such as Bax and Caspase-9, as well as the Akt/I kappa B alpha/NF-kappa B signaling pathway. Consequently, the protective properties of vitamin E establish it as an essential vitamin for the prevention or mitigation of various ACR-induced damages.