Browsing by Author "Gumustekin, Mukaddes"

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The Association of Fc Receptor Polymorphism with Efficacy in Patients With Multiple Sclerosis Treated With Ocrelizumab: A Retrospective Study
(Sage Publications Ltd, 2024) Yigit, Pinar; Gumustekin, Mukaddes; Gurkan, Muharrem Anil; Kaya, Ergi; Ozakbas, Serkan
Effect of Fc-Γ Receptor Polymorphism on the Cognitive Functions in Patients With Multiple Sclerosis Treated With Ocrelizumab: a Retrospective Study
(Sage Publications Ltd, 2024) Yigit, Pinar; Gumustekin, Mukaddes; Gurkan, Muharrem; Ozakbas, Serkan
Ionizing Radiation-Induced Testicular Oxidative Stress and Apoptosis: The Role of Small GTPase RhoA
(Taylor & Francis Ltd, 2025) Manisaligil, Yasar Aysun; Yurt, Aysegul; Ozkan, Cemre Ural; Micili, Serap Cilaker; Sisman, Gizem; Cavdar, Zahide; Gumustekin, Mukaddes
PurposeThe effects of ionizing radiation on living organisms are mainly known as the generation of reactive oxygen species (ROS), apoptosis, and DNA damage. Small GTPases (RhoA, Rac1, Cdc42) are known to have roles in the regulation of oxidative stress and apoptosis. The aim of this study was to investigate the role of the RhoA molecule in testicular tissue damage due to oxidative stress and apoptosis induced by ionizing radiation.Material and methodIn this study, testicular tissues and blood samples obtained from our previous study were examined. In that study, rats were exposed to ionizing radiation at three different doses (0.02 Gy, 0.1 Gy, 5 Gy). Then tissue and blood samples were taken at three different times (2 hours, 24 hours, and 7 days) after irradiation. Immunohistochemical staining was performed to evaluate RhoA and cleaved caspase-3 expressions, while RhoA activity was assessed by G-LISA assay in testicular tissues. Serum malondialdehyde (MDA) levels and superoxide dismutase (SOD) activity were analyzed to evaluate oxidative stress.ResultsThe expression and activation of RhoA demonstrated a time-dependent increase across all levels of radiation doses. Similarly, the expression of cleaved caspase-3 also exhibited a time-dependent increase, consistent with the effects of radiation-induced damage observed in all experimental groups. After exposure to radiation, serum levels of MDA increased, while the activity of SOD decreased.ConclusionOur findings suggest that RhoA may contribute to radiation-induced testicular tissue damage by increasing oxidative stress and apoptosis.
Citation - WoS: 2
Citation - Scopus: 2
Preventative Effect of Montelukast in Mild To Moderate Contrast-Induced Acute Kidney Injury in Rats Via Nadph Oxidase 4, P22phox and Nuclear Factor Kappa-B Expressions
(Springer, 2025) Simsek, Oguzhan; Baris, Elif; Ural, Cemre; Incir, Canet; Aydemir, Selma; Gumustekin, Mukaddes; Arici, Mualla Aylin
Reactive oxygen species (ROS) generation, inflammation and apoptosis are observed in contrast-induced acute kidney injury (CI-AKI). NOX4, isoform of NADPH oxidase main regulatory enzyme for ROS generation, is mostly expressed in the kidney and co-localized with p22phox. It is investigated the effect of antioxidant, anti-inflammatory and anti-apoptotic montelukast pre-treatment on expression of NOX4, p22phox and NF-kappa B in preventing CI-AKI in rats in this study. Wistar male rats randomized into four groups: 1. Control (C), 2. CI-AKI (iohexol; 3 g iodine/kg), 3. Montelukast (10 mg/kg) (M), 4. M + CI-AKI. Rats sacrificed on the 7th day. Urine and serum creatinine and serum Kidney injury molecule-1 (KIM-1) levels measured. NF-kappa B, NOX-4, p22phox mRNA and protein expressions, TNF-alpha, KIM-1 mRNA expressions, ROS and caspase-3 evaluated from kidney tissue. Histological injury scored. ANOVA and Kruskal-Wallis tests were used for analysis parametric and nonparametric data, respectively. p < 0.05 considered statistically significant. Tubular injury score, KIM-1 and caspase-3 levels increased in CI-AKI group compared to C group (p < 0.05). TNF-alpha, NF-kappa B, NOX-4, p22phox, KIM-1 mRNA expressions and ROS levels increased in CI-AKI group compared to C group (p < 0.001 and p < 0.05). NF-kappa B, NOX-4, p22phox protein expressions increased in CI-AKI group compared to C group (p < 0.05) and decreased in the M + CI-AKI group compared to CI-AKI group (p < 0.01, p < 0.05, p < 0.05). TNF-alpha, NF-kappa B, NOX-4, p22phox, KIM-1 mRNA expressions and ROS levels decreased with montelukast pre-treatment (p < 0.001). One of the mechanism of increased ROS level in the CI-AKI model is related the increase the expression of NOX4 and p22phox and montelukast pre-treatment has a protective effect by decreasing NOX4 and p22phox mRNA and protein expressions.
Citation - WoS: 11
Citation - Scopus: 11
Varenicline Prevents Lps-Induced Inflammatory Response Via Nicotinic Acetylcholine Receptors in Raw 264.7 Macrophages
(Frontiers Media Sa, 2021) Baris, Elif; Efe, Hande; Gumustekin, Mukaddes; Arici, Mualla Aylin; Tosun, Metiner
The cholinergic anti-inflammatory pathway plays an important role in controlling inflammation. This study investigated the effects of varenicline, an alpha 7 nicotinic acetylcholine receptor (alpha 7nAChR) agonist, on inflammatory cytokine levels, cell proliferation, and migration rates in a lipopolysaccharide (LPS)-induced inflammation model in RAW 264.7 murine macrophage cell lines. The cells were treated with increasing concentrations of varenicline, followed by LPS incubation for 24 h. Prior to receptor-mediated events, anti-inflammatory effects of varenicline on different cytokines and chemokines were investigated using a cytokine array. Nicotinic AChR-mediated effects of varenicline were investigated by using a non-selective nAChR antagonist mecamylamine hydrochloride and a selective alpha 7nAChR antagonist methyllycaconitine citrate. TNF alpha, IL-1 beta, and IL-6 levels were determined by the ELISA test in cell media 24 h after LPS administration and compared with those of dexamethasone. The rates of cellular proliferation and migration were monitored for 24 h after drug treatment using a real-time cell analysis system. Varenicline decreased LPS-induced cytokines and chemokines including TNF alpha, IL-6, and IL-1 beta via alpha 7nAChRs to a similar level that observed with dexamethasone. Varenicline treatment decreased LPS-induced cell proliferation, without any nAChR involvement. On the other hand, the LPS-induced cell migration rate decreased with varenicline via alpha 7nAChR. Our data suggest that varenicline inhibits LPS-induced inflammatory response by activating alpha 7nAChRs within the cholinergic anti-inflammatory pathway, reducing the cytokine levels and cell migration.