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    Boric Acid Induces Oxidative Damage and Apoptosis Through SEMA3A/PLXNA1/NRP1 Signalling Pathway in U251 Glioblastoma Cell
    (Wiley, 2025) Kar, Ezgi; Ovenler, Zeynep; Hacioglu, Ceyhan; Kar, Fatih
    Glioblastoma is one of the deadliest cancers with a very low chance of survival. Glioblastomas have a poor prognosis because of their infiltrative nature, which makes them difficult to totally isolate with rigorous surgery, radiation, and chemotherapy. Our aim in this study was to investigate the efficacy of boric acid, which has anti-cancer properties, on glioblastoma, which has very limited treatment options. U251 human glioblastoma cell lines were treated with IC25 (15.62 mu g/mL), IC50 (31.25 mu g/mL) and IC75 (62.5 mu g/mL) doses of boric acid. Cell viability and proliferation levels were tested. At the same time, the activity of boric acid on cells was tested through oxidative stress, apoptosis, and semaphorin signalling pathway parameters. Our findings indicate that boric acid induced dose-dependent oxidative stress, cellular growth inhibition, apoptosis and morphological changes in U251 cells. Additionally, treatments with increasing amounts of boric acid resulted in a rise in the production of biomarkers of the semaphorin pathway, which may limit cell growth and proliferation. We found that boric acid activates apoptosis by triggering ROS formation at high doses and at the same time inhibits cell proliferation by increasing semaphorin signalling pathway expressions. Boric acid may act as an anti-cancer agent by activating different mechanisms in a dose-dependent manner.
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    Boric Acid Suppresses Glioblastoma Cellular Survival by Regulating Ferroptosis via SOX10/GPx4/ACSL4 Signalling and Iron Metabolism
    (Wiley, 2025) Kilic, Guven; Hacioglu, Ceyhan; Tuncer, Cengiz; Kar, Ezgi; Kar, Fatih; Taskesen, Ahmet; Kurtulus, Adem
    Ferroptosis, a distinct form of regulated cell death, plays a role in glioma pathogenesis. SRY-box (SOX) transcription factors are key regulators of cancer progression. In this study, we investigated the role of SOX10 in ferroptosis induction in U87 cells following boric acid treatment. First, the cytotoxic effects of boric acid on HMC3 and U87 cells were assessed using CCK8 and BrdU incorporation assays. Subsequently, SOX10, GPX4, ACSL4, GSH, MDA, total ROS, Fe2+, and TFR levels were analysed using ELISA, Western blot, and RT-PCR techniques. Additionally, DAPI staining was performed to evaluate nuclear abnormalities. According to the CCK8 analysis, the IC50 value for boric acid was determined to be 3.12 mM for HMC3 cells and 532 mu M for U87 cells, a finding further supported by BrdU incorporation analysis, which indicated that U87 cells were more sensitive to boric acid. Western blot and RT-PCR analyses revealed that SOX10 expression was significantly higher in U87 cells compared to HMC3 cells. Boric acid treatment led to a reduction in GSH, GPX4, and SOX10 levels in U87 cells, while inducing an increase in MDA, total ROS, ACSL4, Fe2+, and TFR levels. Moreover, microscopic analysis demonstrated that boric acid treatment induced both morphological and nuclear abnormalities in U87 cells. In conclusion, our findings demonstrate that SOX10 is involved in the ferroptosis signalling pathway and that boric acid effectively suppresses U87 cell viability by targeting the SOX10/GPX4/ACSL4 axis.
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    Effects of Curcumin and Boric Acid Against Neurodegenerative Damage Induced by Amyloid Beta (1-42)
    (Humana Press Inc, 2021) Hacioglu, Ceyhan; Kar, Fatih; Kar, Ezgi; Kara, Yakup; Kanbak, Gungor
    Synaptosomes are used as an ex vivo model in the investigation of neuronal transmission and neurodegenerative processes. In this study, we aimed to determine the protective effects of boric acid (BA) and curcumin, which have antioxidant and anti-inflammatory properties, on A beta 1-42 induced neurodegenerative damage. Synaptosomes obtained from the rat cerebral cortex were divided into five groups: control, 10 mu M A beta 1-42, 10 mu M A beta 1-42 + 25 mM BA, 10 mu M A beta 1-42 + 10 mu M curcumin, and 10 mu M A beta 1-42 + 25 mM BA+10 mu M curcumin. Synaptosomes treated with A beta 1-42 caused a significant decline in synaptophysin levels and increase in malondialdehyde (MDA) levels, acetylcholinesterase (AChE) activities, DNA fragmentation values, and nitric oxide (NO) levels compared with the control group (P < 0.01). Synaptosomes treated with BA showed a significant reduction in MDA and NO levels against A beta 1-42 exposure (P < 0.01). In addition, curcumin treatment has been found to cause a significant reduction in AChE activities and MDA levels in synaptosomes (P < 0.05). Co-administration of BA and curcumin on synaptosomes exposed to A beta 1-42 resulted in a significant decrease in DNA fragmentation values, MDA levels, and AChE activities. Curcumin and BA + curcumin combination showed an enhancement in synaptophysin levels of A beta 1-42-induced synaptosomes (P < 0.01). The results showed that BA and curcumin had protective effects on rat brain synaptosomes against A beta 1-42 exposure. BA and curcumin treatment can have abilities to prevent the alterations of the cholinergic system and inhibit oxidative stress in the cerebral cortex synapses of A beta 1-42 exposed.
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    LoxBlock-1 or Curcumin attenuates liver, pancreas and cardiac ferroptosis, oxidative stress and injury in Ischemia/reperfusion-damaged rats by facilitating ACSL/GPx4 signaling
    (Churchill Livingstone, 2023) Kar, Fatih; Yildiz, Fatma; Hacioglu, Ceyhan; Kar, Ezgi; Donmez, Dilek Burukoglu; Senturk, Hakan; Kanbak, Gungor
    In this study, the effects of the pretreatment of Curcumin and LoxBlock-1 on liver, pancreas, and cardiac dysfunction following Ischemia-Reperfusion-induced (IR) Acute Kidney Injury (AKI) were investigated through the mechanisms of oxidative stress and ferroptosis. Total antioxidant status (TAS), total oxidant status (TOS) and oxidative stress index (OSI) parameters in the tissue were analyzed to investigate the oxidative stress occurring in the liver, pancreas, and heart, and Acyl-Coa synthetase long-chain family member (ACSL4). Glutathione peroxidase 4 (GPx4) enzyme levels were also analyzed by ELISA to investigate the effect on ferroptosis. In addition, hematoxylin-eosin staining was performed for histopathological examination of the tissues. As a result of biochemical analyzes, it was observed that oxidative stress parameters increased significantly in the IR group. In addition, while the ACSL4 enzyme level increased in the IR group in all tissues, the GPx4 enzyme level decreased. In the histopathological examination, it was observed that IR caused serious damage to the heart, liver, and pancreas tissues. The present study shows that Curcumin and LoxBlock-1 have a protective effect on the liver, pancreas, and cardiac ferroptosis following the effect on AKI. In addition, Curcumin was found to be more effective than LoxBlock-1 in I/R injury with its antioxidant property.
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    Probiotics ameliorates LPS induced neuroinflammation injury on A beta 1-42, APP, gamma-beta secretase and BDNF levels in maternal gut microbiota and fetal neurodevelopment processes
    (Springer/Plenum Publishers, 2022) Kar, Fatih; Hacıoğlu, Ceyhan; Kar, Ezgi; Donmez, Dilek Burukoglu; Kanbak, Güngör
    The gut microbiota influences brain development and functioning through the gut-brain axis. This is first study regulate maternal gut microbiota and fetal neurodevelopment processes by using probiotics such as Bifidobacterium bifidum (BIF) and Lactobacillus salivarius (LAC) in the prenatal period. In this study, Wistar Albino female rats were divided into five groups; Control, lipopolysaccharide (LPS, 100 mu g/kg), LPS + LAC, LPS + BIF and LPS + LAC + BIF (4 x 10(9) ml CFU). Maternal rats were given probiotics for 21 days. Inflammation was induced by lipopolysaccharide (LPS), on the 17th day of pregnancy. After birth, the brain tissues of the maternal and neonatal rats were removed and their blood was collected. Fecal calprotectin levels of pregnant rats were measured as an important biomarker in determining intestinal flora disruption. Calprotectin levels were high in LPS group (p < 0.05). A beta 1-42, APP, gamma secretase and beta- secretase levels were higher in both maternal and neonatal LPS groups (p < 0.05). These levels were statistically decreased in the probiotic groups compared to the LPS group, as demonstrated in both biochemical and histological analyzes (p < 0.05). While BDNF mRNA expression decreased in LPS groups, APP level increased in the same group. The difference between groups in mRNA expressions in the neonatal brain tissues was similar to maternal brain tissues. What's more, BDNF/actin and APP/actin rates were proven by western blot and the damage caused by neuroinflammation in the brain tissue and the preservation of the intestinal microbiota were visualized histopathologically on the morphological structures in all groups. It will shed light on new therapeutic strategies for the impact of the use of probiotics on the neurodevelopmental processes of the neonatal against LPS-induced inflammatory responses and impaired gut microbiota in the prenatal period.