Yazar "Yanar, Karolin" seçeneğine göre listele

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  • Küçük Resim
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    Caloric restriction and redox homeostasis in various regions of aging male rat brain: Is caloric restriction still worth trying even after early-adulthood? Redox homeostasis and caloric restriction in brain
    (Wiley, 2019) Yanar, Karolin; Şimşek, Bahadır; Çaylı, Nisanur; Bozkır, Haktan Övül; Mengi, Murat; Belce, Ahmet; Çakatay, Ufuk
    Despite recent studies have shown that caloric restriction (CR) could improve some functional loss associated with brain aging, the biochemical effects of CR on brain aging are still not well understood on a quantifiable biochemical basis, including whether CR could be protective when started around middle adulthood, when age-related neurodegenerative diseases are thought to set in. Therefore, in the light of more than ever aging societies and increasing neurodegenerative diseases, we aimed to test the biochemical effects of CR on redox homeostasis in different parts of male Sprague-Dawley rat brain by using the biomarkers we consistently validated in our previous work (TOS, PCO, AOPP, AGEs, sRAGE, P-SH, LHPs, 4-HNE, TAS, Cu, Zn-SOD). Our results indicate that oxidative stress biomarkers are lower in CR group, implying a more favorable redox status that has been previously shown to be correlated with better neural function.
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    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]
  • Küçük Resim Yok
    Öğe
    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, Mehmet
    Metformin 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.