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    Alternations in interleukin-1? and nuclear factor kappa beta activity (NF-kB) in rat liver due to the co-exposure of Cadmium and Arsenic: Protective role of curcumin
    (Elsevier, 2023) Cengiz, Mustafa; Gur, Bahri; Sezer, Canan Vejselova; Cengiz, Betuel Peker; Gur, Fatma; Bayrakdar, Alpaslan; Ayhanci, Adnan
    Cadmium chloride (Cd) and sodium arsenite (As) are two prominent examples of non-biodegradable substances that accumulate in ecosystems, pose a serious risk to human health and are not biodegradable. Although the toxicity caused by individual use of Cd and As is known, the toxicity of combined use (Cd+As) to mammals is poorly understood. The present study aims to investigate the hepatoprotective effect of curcumin (CUR), a naturally occurring bioactive component isolated from the root stem of Curcuma longa Linn., in preventing liver damage caused by a Cd+As mixture. A group of 30 Sprague-Dawley rats were subjected to intraperitoneal administration of Cd+As (0.44 mg/kg+5.55 mg/kg i.p.) and CUR (100 or 200 mg/kg) for a period of 14 days. The experimental results showed that the animals treated with Cd+As exhibited changes in liver biochemical parameters, inflammation and oxidative stress at the end of the experiment. Administration of CUR significantly reduced inflammation, oxidative stress and lipid peroxidation in the Cd+As plus CUR groups compared to the Cd+As group. Furthermore, histological examination of the liver tissue showed that administration of CUR had led to a significant reduction in the liver damage observed in the Cd+As group. The present study provides scientific evidence for the protective effects of CUR against lipid peroxidation, inflammation, oxidative stress and liver damage induced by Cd+As in the liver of rats. The results of our in vivo experiments were confirmed by those of our molecular modelling studies, which showed that CUR can enhance the diminished antioxidant capacity caused by Cd+As.
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    Alternations in nuclear factor kappa beta activity (NF-kB) in the rat brain due to long-term use of atomoxetine for treating ADHD: In vivo and in silico studies
    (Academic Press Inc Elsevier Science, 2021) Gur, Fatma; Cengiz, Mustafa; Gur, Bahri
    Attention Deficit Hyperactivity Disorder (ADHD) is the most common psychiatric disorder reported particularly in children. Long-term use of antipsychotic drugs used in the treatment of ADHD has been shown to exert toxic effects on the brain. However, not enough research has been carried out on the neurotoxic effects of these drugs on the brain tissue. Atomoxetine (ATX) is the most widely used antipsychotic drug that has gained approval for ADHD treatment. The present study aims to determine the damage induced by long-term use of three different doses of ATX in the brain tissue of experimental rats. 24 rats were divided into Control group (0.5 mL saline), Group 2 (0.5 mg/mL ATX), Group 3 (1.0 mg/mL ATX), and Group 4 (2.0 mg/mL ATX), each group having 6 members. Their brain tissues were taken for stereological, histological, and nuclear factor kappa-B (NF-kB) protein expression analysis. ATX was determined to have caused a few alterations in the brain tissue, such as disruption in the endothelial epithelium of capillaries, a couple of large astrocyte nuclei, and mitotic astrocytes. Moreover, a significant difference was observed in Group 4 compared to Control Group in terms of astrocyte counts in the brain sections. As for Groups 3 and 4, there were differences in terms of oligodendrocyte counts in the incisions cultivated from the brain tissues of the animals. On the other hand, NF-kB positive astrocytes of Groups 3 and 4 differed significantly from those of Control and Group 2. The results of molecular dockings of the present study are in line with the in-vivo results. Therefore, it was concluded that the higher the dose of ATX was, the more damage the brain tissue sustained. (c) 2020 Elsevier Inc. All rights reserved.
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    Decreased Na+/K+ pump activity in the erythrocyte membrane due to malondialdehyde in rheumatoid arthritis: an in vivo and in silico study
    (Canadian Science Publishing, 2022) Ogul, Yasemin; Gur, Fatma; Gur, Bahri; Cengiz, Mustafa; Sari, Refik Ali; Kiziltunc, Ahmet
    Apart from demonstrating the interaction behavior of malondialdehyde (MDA) with Na+/K+-ATPase using in silico, the current study aims to investigate the effect of rheumatoid arthritis-related oxidative stress on Na+/K+-ATPase activity that is present in the erythrocyte cell membrane, which is rich in proteins vulnerable to damage from MDA and other free radicals. The target population of this study consists of 28 rheumatoid arthritis patients and 20 healthy volunteers whose MDA levels and Na+/K+-ATPase activity were determined. It was shown that MDA levels of rheumatoid arthritis patients increased (p < 0.001) and their Na+/K+-ATPase activity noticeably decreased when compared to those of healthy individuals. Also, according to this in silico modeling, MDA decreased Na+/K+-ATPase activity in line with the correlation analyses. Consequently, while elevated levels of MDA in the rheumatoid arthritis group were suggestive of oxidative stress, a decreased Na+/K+-ATPase-activity led us to speculate that the cellular membrane had sustained injury. Therefore, our results could be useful in explaining how MDA affects Na+/K+-ATPase activity in the interior of a specific molecular pathway.
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    Evaluation of oxidant and intracellular anti-oxidant activity in rheumatoid arthritis patients: In vivo and in silico studies
    (Elsevier, 2021) Ogul, Yasemin; Gur, Fatma; Cengiz, Mustafa; Gur, Bahri; Sari, Refik Ali; Kiziltunc, Ahmet
    Rheumatoid Arthritis (RA) is the most prevalent cause of the systematic inflammatory arthritis that destroys the joints. While the pathogenesis of RA remains to be clarified, the imbalance in the oxidant and anti-oxidant defense system plays a crucial role. This study aims to evaluate oxidant and anti-oxidant levels of RA patients and their impacts on the activity of the disease via in silico studies. 28 patients who had not previously received any treatment for RA and 20 healthy controls were included. Their oxidative stress markers, antioxidant markers, and inflammatory factors were investigated via in silico studies. Compared to the Control Group, serum CRP levels, MDA levels, and XO activities were higher in RA Group. Cu/ZnSOD and GPx activities decreased while CAT activities remained unchanged. Besides, there was a positive correlation between MDA-serum CRP levels but a negative correlation between MDA levels-Cu/ZnSOD activities. Furthermore, we observed a negative correlation between CRP levels and Cu/ZnSOD activities. Based on these results, it was concluded that oxidative stress had increased, the defense system had weakened, and ROS production had increased. Finally, our study results with SOD and CAT activity were confirmed by molecular docking studies.
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    Molecular docking analyses of Escin as regards cyclophosphamide-induced cardiotoxicity: In vivo and in Silico studies
    (Academic Press Inc Elsevier Science, 2021) Gur, Fatma; Cengiz, Mustafa; Kutlu, Hatice Mehtap; Cengiz, Betul Peker; Ayhanci, Adnan
    This study aims to investigate whether Escin (ES) can protect against Cyclophosphamide (CPM)-induced cardiac damage. The experimental rats were categorized as Control, CPM (200 mg/kg), ES (10 mg/kg), and CPM + ES Groups, each having 6 members. Their heart tissues were stained with Hematoxylin and Eosin and the structural changes were investigated under the light microscope. The biochemical markers of ischemia modified albumin (IMA), creatine kinase (CK-MB), antioxidant activity indicators Catalase (CAT), and superoxide dismutase (SOD) activities were measured using blood samples. Besides, the effects of CPM, ES, and CPM + ES upon CAT and SOD activities were shown via molecular docking studies. In the Single-Dose CPM group, CK-MB and IMA levels significantly increased while SOD and CAT levels significantly decreased. However, the heart tissues were damaged. CK-MB and IMA levels significantly decreased in CP+ ES Group. On the other hand, SOD, and CAT levels significantly increased and reduced the damage remarkably. Our findings showed that ES treatment successfully reduced the toxic effects upon the rats. The conclusion is that ES treatment can help protect the heart tissue against CPM-induced toxicity. Both in-vivo results and molecular modeling studies showed that the negative effects of CPM upon SOD activity were bigger than that of CAT.
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    The role of Bax/Bcl-2 and Nrf2-Keap-1 signaling pathways in mediating the protective effect of boric acid on acrylamide-induced acute liver injury in rats
    (Pergamon-Elsevier Science Ltd, 2022) Cengiz, Mustafa; Ayhanci, Adnan; Akkemik, Ebru; Sahin, Ilknur Kulcanay; Gur, Fatma; Bayrakdar, Alpaslan; Cengiz, Betul Peker
    Introduction: This study aims to investigate whether boric acid (BA) can protect rats from acrylamide (AA)induced acute liver injury. Materials and methods: AA was used to induce acute liver injury. Thirty rats were divided into five group including Group 1 (saline), Group 2 (AA), Group 3 (20 mg/kg BA), Group 4 (10 mg/kg BA+AA) and Group 5 (20 mg/kg BA+AA). Their blood and liver were harvested to be kept for analysis. Liver function enzyme activities were performed by spectrophotometric method. Catalase (CAT), superoxide dismutase (SOD) activity, and malondialdehyde levels were determined by colorimetric method. The in-silico studies were performed using the blind docking method. Results: Administration AA to rats, biochemical parameters, liver histology, and expression levels of apoptotic markers were negatively affected. However, after the administration of BA, the altered biochemical parameters, liver histology, and expression levels of apoptotic markers were reversed. Moreover, the mechanisms of AA-induced deterioration in the levels of SOD, CAT, and Nrf2-Keap-1 and the mechanisms of the protective effect of BA against these deteriorations were explained by in silico studies. Conclusion: Thus, the present study could explain the interactions between AA and thiol-containing amino acid residues of Keap-1, the effect of BA on these interactions, and the biochemical toxicity caused by the AA. In this sense, this work is the first of its kind in the literature. Based on the biochemical, histopathological, and in silico results, it can be suggested that BA has the potential to be used as a protective agent against AA-induced liver injury.
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    Therapeutic role of boron on acrylamide-induced nephrotoxicity, cardiotoxicity, neurotoxicity, and testicular toxicity in rats: Effects on Nrf2/Keap-1 signaling pathway and oxidative stress
    (Elsevier Gmbh, 2023) Gur, Fatma; Cengiz, Mustafa; Gur, Bahri; Cengiz, Osman; Saricicek, Osman; Ayhanci, Adnan
    Background: Acrylamide (ACR) is a heat-related carcinogen used in cooking some foods as well as in other thermal treatments. The present study aims to investigate the possible protective effect of boron (BA) against ACR-induced toxicity of kidney, brain, heart, testis, and bladder tissues in rats. Methods: Rats have been divided into 5 equal groups: Control (saline), ACR (38.27 mg/kg), BA (20 mg/kg), BA+ ACR (10 mg/kg + ACR), and BA+ ACR (20 mg/kg BA+ACR). Kidney tissue from rats was collected and the levels of malondialdehyde (MDA), glutathione (GSH), and the activity of superoxide dismutase (SOD) were measured. In addition, the kidneys of these animals, as well as the brain, heart, testes, and bladder tissues were examined for possible histological changes. Total Nrf2 and Keap-1 protein expression in kidney, heart, and testis tissues was examined by immunohistochemistry. Results: While significant increases in MDA levels were observed in the kidneys of rats receiving ACR alone, significant decreases in antioxidant markers (SOD and GSH) were observed. Besides, kidney, brain, heart, and testicular tissues were analyzed and damage was observed in the groups receiving ACR. However, no significant histologic changes were noted in the bladder tissue. Both dosages of BA in combination with ACR improved the changes in ACR-induced antioxidant tissue parameters. Despite the fact that MDA levels were decreased with these two dosages, histological structural abnormalities were found to be greatly improved. Conclusion: Our results show that BA has a strong protective effect on ACR-induced multi-organ toxicity. The study results show that BA could be a potential element to reduce ACR toxicity to which we are often exposed.