Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection
Permanent URI for this collectionhttps://hdl.handle.net/11147/7148
Browse
5 results
Search Results
Now showing 1 - 5 of 5
Article Epigallocatechin Gallate and Punicalagin Combination Reduces Aβ Aggregation and Promotes Neurogenesis in Adult Zebrafish Brain(John Wiley and Sons Inc, 2026) Nazli, D.; Ipekgil, D.; Poyraz, Y.K.; Can, K.; Okmen, I.; Turhanlar-Sahin, E.; Ozhan, G.Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline, memory impairment, and behavioral alterations. The pathogenesis of AD involves the accumulation of amyloid-beta (Aβ) plaques and the hyperphosphorylated tau proteins, which disrupt neuronal function and trigger neuroinflammation. This study explores the therapeutic potential of epigallocatechin gallate (EGCG) and punicalagin (PU) in mitigating Aβ-induced toxicity using an adult zebrafish model of AD. Our results demonstrate that the EGCG + PU combination significantly reduces Aβ accumulation, protects against cellular damage, suppresses acetylcholinesterase (AChE) activity, and normalizes the expression of amyloidogenic and AD-related genes. Additionally, EGCG + PU treatment alleviates neuroinflammation by suppressing glial activation, including reductions in L-plastin and proinflammatory cytokine expression, while promoting neuronal recovery through mechanisms of neurogenesis and neuroprotection. Notably, the combination treatment restored neuronal density and improved behavioral outcomes by alleviating anxiety- and aggression-like behaviors associated with Aβ toxicity. These results underscore the synergistic neuroprotective effects of EGCG + PU, highlighting their potential as a novel therapeutic approach for mitigating the pathological, behavioral, and inflammatory aspects of AD. © 2026 Wiley Periodicals LLC.Article Notum1a Inhibition Promotes Neurogenesis in the Adult Zebrafish Brain(Nature Portfolio, 2025) Kocagoz, Yigit; Erdogan, Nuray Sogunmez; Ozdinc, Sevval; Ipekgil, Dogac; Katkat, Esra; Ozhan, GunesNotum is a carboxylesterase enzyme that modulates extracellular signaling by hydrolyzing palmitoleoyl residues from proteins, thereby influencing key pathways involved in cell differentiation, survival, and proliferation. While notum1 expression has been identified in the brain, its role in adult neurogenesis remains poorly understood. Using the adult zebrafish brain as a model system, we demonstrate that the notum1a homolog is broadly expressed across various brain cell types but is absent in undifferentiated radial glial cells. Pharmacological inhibition of Notum activity with the small molecule inhibitor ABC99 stimulates activation of radial glial cells, leading to increased neurogenesis. A BrdU pulse-chase assay confirms that ABC99-induced proliferation enhances the production of mature neurons. Despite Notum's established role in Wnt signaling, transcriptional analysis following ABC99 treatment reveals no sustained impact on Wnt pathway targets, suggesting that Notum may regulate neurogenesis through alternative mechanisms. Our findings highlight notum1a as a potential modulator of neural progenitor cell dynamics in the adult brain and suggest that targeting Notum could represent a novel therapeutic strategy for neurodegenerative conditions characterized by impaired neurogenesis.Article Citation - WoS: 2Citation - Scopus: 2Tuning Toxicity Profiles of Graphene Oxide Through Imidazole-Oxime Modification: Zebrafish as a Model System(Oxford Univ Press, 2025) Yildirim, Serkan; Kokturk, Mine; Yigit, Aybek; Sahin, Ayse; Kiliclioglu, Metin; Atamanalp, Muhammed; Alak, GoncaThe increasing use of nanotechnology, especially in agriculture and the food industry, has raised concerns about the possible adverse effects of nanomaterials (NMs) on human health and the environment. This study investigates the effects of synthesized graphene oxide (GO) and its derivatives on zebrafish exposed for 96 hr, focusing on morphological changes in brain tissue, histopathology, and immunofluorescent markers such as 8-hydroxy-2'-deoxyguanosine (8-OHdG) and nucleolar protein 10 (NOP10). Exposure to GO resulted in malformations, DNA damage, and increased NOP10 expression, and it reduced hatching and survival rates. Our results demonstrated that exposure to GO, graphene oxide-oxime (GO-OX), and OX exerted dose-dependent inhibitory effects on hatching and promoted malformations in zebrafish larvae. Histopathological analysis revealed that higher doses led to more pronounced tissue damage, with GO 50 causing severe degeneration and necrosis, while high doses of GO-OX and OX resulted in moderate tissue changes. This was further supported by the increased expression levels of 8-OHdG (marker of oxidative DNA damage) and NOP10 (marker of nucleolar stress), which aligns with the histopathological findings and confirms the neurotoxic effects. Notably, GO-OX treatments consistently mitigated both morphological and neurotoxic effects at all doses, suggesting that oxime functionalization reduces the inherent toxicity of GO. In contrast, treatment with different concentrations of GO-OX derivatives mitigated these adverse effects, reducing them to mild or moderate levels.Review Citation - Scopus: 2Wnt/β-catenin Signaling in Central Nervous System Regeneration(2025) Nazli, D.; Bora, U.; Ozhan, G.The Wnt/β-catenin signaling pathway plays a pivotal role in the development, maintenance, and repair of the central nervous system (CNS). This chapter explores the diverse functions of Wnt/β-catenin signaling, from its critical involvement in embryonic CNS development to its reparative and plasticity-inducing roles in response to CNS injury. We discuss how Wnt/β-catenin signaling influences various CNS cell types-astrocytes, microglia, neurons, and oligodendrocytes-each contributing to repair and plasticity after injury. The chapter also addresses the pathway's involvement in CNS disorders such as Alzheimer's and Parkinson's diseases, psychiatric disorders, and traumatic brain injury (TBI), highlighting potential Wnt-based therapeutic approaches. Lastly, zebrafish are presented as a promising model organism for studying CNS regeneration and neurodegenerative diseases, offering insights into future research and therapeutic development. © 2024. The Author(s), under exclusive license to Springer Nature Switzerland AG.Article Gypsophila Eriocalyx Roots Inhibit Proliferation, Migration, and Tgf-Β Signaling in Melanoma Cells(Walter de Gruyter GmbH, 2025) Azbazdar, Yagmur; Ozhan, Gunes; Helvacioglu, SelinObjectives: Melanoma is a highly malignant and serious form of skin cancer. In addition to the standard treatments, complementary approaches, including phytotherapy, are also used to alleviate symptoms and improve patient well- being. This study aims to investigate the anticancer effects of Gypsophila eriocalyx (GE), an endemic species from Türkiye, on melanoma cells. We set out to determine the efficacy of GE in inhibiting melanoma cell proliferation, migration, and growth, and to explore its underlying mechanisms. Methods: We examined the impact of GE on the prolifera- tion of two melanoma cell lines, Malme-3M and SK-MEL-28, and assessed its developmental toxicity in zebrafish em- bryos. Next, we evaluated GE’s influence on colony forma- tion and wound healing in melanoma cells, as well as its ability to induce apoptosis and affect the TGF-β/Smad signaling pathway, by measuring pathway reporter activity and target gene expression. Results: GE inhibited cell proliferation in melanoma cell lines at concentrations 104 to 488 times lower than those required for normal non-malignant L929 fibroblast cells. In zebrafish embryos, GE demonstrated developmental toxicity only at concentrations above 50 μg/mL. GE treatment significantly impaired the colony formation and wound healing abilities of melanoma cells, indicating reduced pro- liferation and migration. Moreover, GE induced apoptosis in melanoma cells and inhibited the TGF-β/Smad signaling pathway, as evidenced by decreased pathway reporter activity and target gene expression. Conclusions: This study highlights the potential of GE as a novel therapeutic agent in melanoma treatment by demon- strating its ability to inhibit tumor growth and progression