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    NEUROPROTECTIVE EFFECT OF CHLORZOXAZONE AGAINST GLUTAMATE TOXICITY IN RAT PRIMARY CORTEX NEURON CULTURE
    (2024) Yeni, Yeşim; ÇIÇEK, BETÜL; Hacimuftuoglu, Ahmet
    Glutamate (Glut) toxicity is one of the main causes of neurological diseases. Chlorzoxazone (CZ) is a muscle relaxant used to decrease pain and inflammation associated with acute and chronic twists and bruises. Here, we objected to research the neuroprotective effect of CZ applied to reverse Glut-induced neurodegeneration in the neonatal cerebral cortex through anti-inflammatory and antioxidant mechanisms. Neonatal cortical neurons were exposed to Glut and different doses of CZ (10, 20, and 40 µM) were applied to assess the effect of CZ on Glut toxicity. We then examined changes in cell viability, inflammation, and oxidative stress. Our cell viability analysis showed that CZ protected cells from Glut-induced neuronal damage. In addition, the neuroprotective properties of CZ were evaluated by examining oxidative and antioxidant parameters such as MDA, MPO, CAT, GSH, GPx, and SOD. In line with the data obtained, it was observed that the cell viability rate decreased to 60% in the Glut group. However, with CZ application, the most significant increase in cell viability was seen at the 40 ?M dose (86%), while the least increase was seen at 10 ?M CZ (77%). It also proved that CZ increased the activity of antioxidant parameters while reducing oxidative parameters and inflammation. Therefore, the present findings collectively demonstrated that CZ potently inhibits Glut-induced injury in neonatal cortical neurons. The present work is the initial to show the protective effect of CZ in neonatal cortical neurons exposed to Glut excitotoxicity and suggesting that CZ may be used as a therapeutic agent.
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    Nicorandil mitigates glutamate excitotoxicity in primary cultured neurons
    (2024) ERTUGRUL, MUHAMMED SAIT; Okkay, Ufuk; Yeni, Yeşim; Genç, Sıdıka; Balpınar, Özge; Okkay, Irmak Ferah; Hacimuftuoglu, Ahmet
    Excitotoxicity, caused by the excessive release of glutamate, leads to the activation of the apoptotic process, making it a crucial factor in age-related neurodegenerative diseases. The aim of this study was to investigate the potential of nicorandil to prevent glutamate excitotoxicity and reduce oxidative stress in the brain by analyzing the effects of nicorandil on primary cortex neurons. The study used primary neuron cultures from newborn Sprague-Dawley rats to examine the impact of nicorandil on cell viability, Superoxide Dismutase, Catalase, Glutathione activity, Malondialdehyde levels, total antioxidant capacity, and total antioxidant status of neurons subjected to glutamate-induced excitotoxicity. Nicorandil at varying concentrations was introduced in the culture to assess its protective effects on the neurons. The results showed that nicorandil significantly improved cell viability and total antioxidant capacity levels and reduced total antioxidant status values in a concentration-dependent manner. These findings indicate that nicorandil effectively prevented glutamate excitotoxicity by reducing oxidative stress. The study suggests that nicorandil holds the potential for treating neurodegenerative diseases caused by glutamate excitotoxicity. This study is the first to report the potential of nicorandil to inhibit oxidative stress and prevent glutamate excitotoxicity in primary neurons, providing a basis for further exploration of the clinical application of nicorandil in neurodegenerative diseases.
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    Wound Healing of Quinic Acid in Human Dermal Fibroblasts by Regulating Expression of FN1 and COL1A1 Gene
    (2022) Genç, Sıdıka; ÇIÇEK, BETÜL; Yeni, Yeşim; Hacimuftuoglu, Ahmet
    Quinic acid (QA) is an alicyclic organic acid widely found in plants. It accumulates in varying concentrations of plant species and is actively metabolized throughout the plant's life cycle. Wound healing after skin injury involves a complex interaction of many cells, fibroblasts, endothelial cells, and regenerated immune cells and their interrelating extracellular matrix. In our study, the healing effect of QA on scar tissue was studied. For this aim, oxidative stress, and changes in FN1 and Collogen1? gene levels were examined. For this purpose, fibroblast cells were seeded in 24, 96 and well plates for wound healing, MTT analysis and Real-Time PCR testing (respectively). Wells were drawn with a 100 µL pipette tip for wound line. As a conclusion of our study, it was determined that cell viability increased significantly, especially in the QA 20 µg-ml group at the end of 48 hours. Increased cell viability and antioxidant capacity resulted in increased cell proliferation. Both FN1 and COL1A1 gene expression levels were up regulated in the QA groups compared to the control group. Our findings show for the first time that quinic acid promotes migration and/or proliferation of fibroblasts by regulating oxidative stress and the FN1A and COL1A1 genes. This activity may be related to the production of FN1A and COL1A1, which are considered important targets for modulation of the tissue repair process.