Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection

Permanent URI for this collectionhttps://hdl.handle.net/11147/7148

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  • Article
    K41-A Enhances the Antiproliferative Efficacy of Cisplatin in Neuroblastoma by Modulating Apoptosis and Autophagy
    (Oxford University Press, 2026) Sanlav, Gamze; Kum Ozsengezer, Selen; Altun, Zekiye; Bedir, Erdal; Aktas, Safiye; Olgun, Nur
    Objectives Neuroblastoma (NB), the most common extracranial tumor in childhood, has a poor prognosis, especially in cases with MYC gene amplification. Cisplatin (CDDP) is widely used in treatment, but its effectiveness is limited due to chemotherapy resistance. Autophagy plays a dual role in cancer progression, either promoting survival or contributing to cell death.Methods This study explores the anticancer effects of K41-A, a polycyclic polyether molecule, alone and in combination with CDDP in SH-SY5Y and KELLY NB cell lines, the HE-IOC1 noncancerous cochlear cell line, and the NB xenograft model.Key findings For the first time, we demonstrate that K41-A, either alone or combined with CDDP, significantly inhibits cell proliferation selectively in NB cells, sparing noncancerous cells. This study confirmed that K41-A alone and in combination with CDDP induced changes in both apoptotic and autophagic cell death components in NB, resulting in antiproliferative activity in vitro and in vivo. In addition, the combination with CDDP enhanced the therapeutic efficacy of K41-A.Conclusions These results highlight the potential of K41-A as a candidate drug for the treatment of NB.
  • Article
    Citation - WoS: 3
    Citation - Scopus: 3
    Evaluation of the Effects of Carbamazepine-Loaded Chitosan-Coated Plga-Zein Nanoparticles on Pilocarpine-Induced Seizure Model in Zebrafish Larvae: Developmental Toxicity and Behavioral Assays
    (Oxford University Press, 2025) Alak, G.; Yıldırım, S.; Ugur Kaplan, A.B.; Köktürk, M.; Nazli, D.; Gözegir, B.; Cetin, M.
    Epilepsy, the most common neurological disorder worldwide, is characterized by sudden paroxysmal brain activity, which can be generalized or focal. Extensive research has explored various treatment strategies for this condition. Our study used a pilocarpine (PL)-induced seizure model in zebrafish (Danio rerio) embryos and larvae to assess the effects of carbamazepine (CBZ)-loaded chitosan-coated PLGA-Zein nanoparticles (NPs) over 96 hr. We evaluated the developmental toxicity (mortality, malformation, and larval hatching), behavioral changes (sensorimotor reflexes), and histopathological and immunohistochemical alterations in brain tissue, focusing on 5-hydroxytryptamine receptor 4 (5HT4), and brain and muscle ARNT-like 1 (BMAL1) expressions. Our findings revealed high mortality and malformation rates in groups treated with pure CBZ (PL + CBZ 50 and PL + CBZ 100). These groups also exhibited delayed hatching and impaired sensorimotor reflexes. In contrast, the CBZ-NP-treated groups (PL + CBZ NP 50 and PL + CBZ NP 100) showed hatching rates comparable with the control group, with significantly lower mortality and malformation rates compared with pure CBZ-treated groups. Moreover, intense cytoplasmic expression of 5HT4 and BMAL1 was observed in neuropils of the PL + CBZ 100 group. This study highlights the potential of CBZ-loaded NPs in reducing developmental toxicity and adverse neurological effects associated with pure CBZ treatment in seizure models. © The Author(s) 2025. Published by Oxford University Press on behalf of the Society of Environmental Toxicology and Chemistry. All rights reserved.
  • Article
    Citation - WoS: 88
    Citation - Scopus: 92
    Sur1-Trpm4 Cation Channel Expression in Human Cerebral Infarcts
    (Oxford University Press, 2015) Mehta, Rupal I.; Tosun, Çiğdem; Ivanova, Svetlana; Tsymbalyuk, Natalia; Famakin, Bolanle M.; Kwon, Min Seong; Castellani, Rudy J.; Gerzanich, Volodymyr; Simard, J. Marc
    The nonselective monovalent cation channel transient receptor potential melastatin 4 (Trpm4) is transcriptionally upregulated in neural and vascular cells in animal models of brain infarction. It associates with sulfonylurea receptor 1 (Sur1) to form Sur1-Trpm4 channels, which have critical roles in cytotoxic edema, cell death, blood-brain barrier breakdown, and vasogenic edema. We examined Trpm4 expression in postmortem brain specimens from 15 patients who died within the first 31 days of the onset of focal cerebral ischemia. We found increased Trpm4 protein expression in all cases using immunohistochemistry; transcriptional upregulation was confirmed using in situ hybridization of Trpm4 messenger RNA. Transient receptor potential melastatin 4 colocalized and coassociated with Sur1 within ischemic endothelial cells and neurons. Coexpression of Sur1 and Trpm4 in necrotic endothelial cells was also associated with vasogenic edema indicated by upregulated perivascular tumor necrosis factor, extravasation of serum immunoglobulin G, and associated inflammation. Upregulated Trpm4 protein was present up to 1 month after the onset of cerebral ischemia. In a rat model of middle cerebral artery occlusion stroke, pharmacologic channel blockade by glibenclamide, a selective inhibitor of sulfonylurea receptor, mitigated perivascular tumor necrosis factor labeling. Thus, upregulated Sur1-Trpm4 channels and associated blood-brain barrier disruption and cerebral edema suggest that pharmacologic targeting of this channel may represent a promising therapeutic strategy for the clinical management of patients with cerebral ischemia.