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Öğe Protective effect of Apelin-13 on D-glutamic acid-induced excitotoxicity in SH-SY5Y cell line: An in-vitro study(Churchill Livingstone, 2025) Oruç, Kadriye Yağmur; Ağtürk, Gökhan; Oruç, Aykut; Yanar, Karolin; Seymen, Hakkı OktayExcitotoxicity, resulting from excessive accumulation of glutamate in the extracellular space, leads to neuronal cell death. This study investigates the protective effects of Apelin-13 on D-Glutamic acid-induced excitotoxicity in SH-SY5Y human neuroblastoma cells, an in-vitro model for neurodegenerative diseases. Unlike the commonly studied L-glutamic acid, this research focuses on D-Glutamic acid to understand its specific impacts. SH-SY5Y cells were treated with varying concentrations of D-Glutamic acid and Apelin-13, followed by analyses at 12 and 24 h to evaluate cell viability, oxidative stress markers, and inflammatory cytokine levels. Cell viability assays revealed significant cytotoxic effects of D-Glutamic acid at doses of 10 mM and 20 mM, reducing viability by over 50 %. However, Apelin-13 treatment mitigated these effects, especially at 2 μg/ml, enhancing cell viability and reducing inflammatory cytokine levels (IL-1β and TNF-α). Apelin-13 also increased anti-inflammatory cytokine levels (IL-10 and TGF-β1) and brain-derived neurotrophic factor (BDNF), indicating its neuroprotective role. Oxidative stress markers, including ROS, AGE, AOPP, DT, T-SH, were significantly elevated by D-Glutamic acid but effectively reduced by Apelin-13. The neuroprotective mechanisms of Apelin-13 involve modulation of cAMP/PKA and MAPK signaling pathways, enhancing BDNF synthesis and suppressing oxidative stress and inflammatory responses. This study is the first to demonstrate the effects of D-Glutamic acid on SH-SY5Y cells. It highlights Apelin-13's potential as a therapeutic agent against excitotoxicity-induced neuronal damage, emphasizing its ability to modulate key molecular pathways involved in inflammation and oxidative stress. Further in-vivo studies are warranted to explore the long-term neuroprotective effects of Apelin-13 in treating neurodegenerative diseases. © 2024Öğe The Role of Glycogen Synthase Kinase-3? in the Zinc-Mediated Neuroprotective Effect of Metformin in Rats with Glutamate Neurotoxicity(Springernature, 2024) Oruc, Aykut; Oruc, Kadriye Yagmur; Yanar, Karolin; Mengi, Murat; Caglar, Aysel; Kurt, Bahar Ozturk; Altan, MehmetMetformin has been suggested to have protective effects on the central nervous system, but the mechanism is unknown. The similarity between the effects of metformin and the inhibition of glycogen synthase kinase (GSK)-3 beta suggests that metformin may inhibit GSK-3 beta. In addition, zinc is an important element that inhibits GSK-3 beta by phosphorylation. In this study, we investigated whether the effects of metformin on neuroprotection and neuronal survival were mediated by zinc-dependent inhibition of GSK-3 beta in rats with glutamate-induced neurotoxicity. Forty adult male rats were divided into 5 groups: control, glutamate, metformin + glutamate, zinc deficiency + glutamate, and zinc deficiency + metformin + glutamate. Zinc deficiency was induced with a zinc-poor pellet. Metformin was orally administered for 35 days. D-glutamic acid was intraperitoneally administered on the 35th day. On the 38th day, neurodegeneration was examined histopathologically, and the effects on neuronal protection and survival were evaluated via intracellular S-100 beta immunohistochemical staining. The findings were examined in relation to nonphosphorylated (active) GSK-3 beta levels and oxidative stress parameters in brain tissue and blood. Neurodegeneration was increased (p < 0.05) in rats fed a zinc-deficient diet. Active GSK-3 beta levels were increased in groups with neurodegeneration (p < 0.01). Decreased neurodegeneration, increased neuronal survival (p < 0.01), decreased active GSK-3 beta ( p < 0.01) levels and oxidative stress parameters, and increased antioxidant parameters were observed in groups treated with metformin (p < 0.01). Metformin had fewer protective effects on rats fed a zinc-deficient diet. Metformin may exert neuroprotective effects and increase S-100 beta-mediated neuronal survival by zinc-dependent inhibition of GSK-3 beta during glutamate neurotoxicity.Öğe Role of Reelin and Zinc in the Pathogenesis of D-Glutamic Acid-Induced PAH(Wiley, 2023) Oruc, Kadriye Yagmur; Oruc, Aykut; Altan, Mehmet; Sonmez, Osman Fuat; Yanar, Karolin; Kepil, Nuray; Mengi, Murat[Abstract Not Available]Öğe The neuroinflammatory and neuroprotective roles of apelin-13 in d-glutamic acid-induced excitotoxicity in SH-SY5Y cell line(Wiley, 2025) Oruç, Kadriye Yağmur; Ağtürk, Gökhan; Oruç, Aykut; Yanar, Karolin; Seymen, Hakkı OktayThe neuroinflammatory and neuroprotective roles of apelin-13 in d-glutamic acid-induced excitotoxicity in SH-SY5Y cell line
