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    Antiproliferative and apoptotic effects of Pervari honey on SH-SY5Y neuroblastoma cells
    (Humana Press Inc, 2025) Altin-Celik, Pinar; Derya-Andeden, Muazzez; Eciroglu-Sarban, Hamiyet; Donmez-Altuntas, Hamiyet
    Neuroblastoma is a complex and heterogeneous pediatric malignancy. Treatment options for neuroblastoma include surgery, chemotherapy, radiotherapy, autologous stem cell transplantation, and emerging immunotherapies. However, these approaches often coincide with oxidative stress, highlighting the potential role of natural antioxidants in chemoprevention and chemotherapy. Honey has long been recognized for its medicinal properties, including antimicrobial, anti-inflammatory, and antioxidant effects. Pervari honey (PH), produced by bees that forage on a diverse array of native flora, is a distinctive honey originating from southeastern T & uuml;rkiye. This study evaluated the antiproliferative, anti-tumor, apoptotic, and inflammatory effects of PH on SH-SY5Y human neuroblastoma cells. Cell viability was measured using an MTT assay, while apoptosis was evaluated using an Annexin V-FITC/7-AAD staining test. The RT-qPCR method was used to quantify the expression of IL-1 beta, IL-6, TNF-alpha, NF-kappa B, Caspase-3, MMP-2, MMP-9, BAX, and BCL-2 genes. PH significantly reduced SH-SY5Y cell viability in a dose- and time-dependent manner (p < 0.05-p < 0.01). It induced apoptosis by upregulating BAX and Caspase-3 while downregulating BCL-2 (p < 0.05-p < 0.001). Additionally, it increased NF-kappa B expression (p < 0.05-p < 0.001) and modulated inflammatory (IL-1 beta, IL-6, and TNF-alpha) cytokines (p < 0.05-p < 0.01). MMP-2 and MMP-9 levels were significantly elevated (p < 0.05-p < 0.001), suggesting enhanced extracellular matrix remodeling. These in vitro findings indicate that PH may exert anti-tumor potential and possess immunomodulatory properties. Furthermore, in vitro and in vivo studies are needed to explore its therapeutic applicability.
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    Neuroprotective Effects of Hesperidin and CK2 Inhibitor DRB on A?1-42-Induced Neurotoxicity in Differentiated SH-SY5Y Cells
    (Springer, 2025) Eciroglu-Sarban, Hamiyet; Altin-Celik, Pinar; Kelicen-Ugur, Pelin; Donmez-Altuntas, Hamiyet
    There is still no approved treatment for Alzheimer's disease (AD), a progressive neurodegenerative disorder characterized by amyloid plaques, neurofibrillary tangles, and synaptic dysfunction. In an in vitro AD model, this study aimed to comparatively assess the neuroprotective effects of the citrus flavonoid Hesperidin and the casein kinase 2 (CK2) inhibitor 5,6-dichloro-1-beta-D-ribofuranosyl benzimidazole (DRB) as potential therapeutic targets for AD. First, SH-SY5Y neuroblastoma cells were differentiated into cholinergic neuron-like cells using all-trans retinoic acid (RA) and brain-derived neurotrophic factor (BDNF). Then, to generate an in vitro AD model, 20 mu M A beta(1-42) was applied to induce neurotoxicity in differentiated SH-SY5Y cells. The neuroprotective effects of the CK2 inhibitor DRB and Hesperidin on the in vitro AD model were evaluated using MTT, RT-qPCR, and ELISA methods. Both Hesperidin and DRB, at high concentrations, reduced cell viability in differentiated SH-SY5Y cells for 24 and 48 h (p < 0.05 to p < 0.01). Pre-treatment with Hesperidin at 25 and 50 mu M and DRB at 0.25 and 0.5 mu M for 24 h increased ADAM10 gene expression and decreased BACE1 gene expression, both of which are associated with AD markers, compared to the 20 mu M A beta(1-42) treatment group (p < 0.05). Pre-treatment with the DRB at 0.25 and 0.5 M concentrations for 24 h decreased CK2 alpha gene expression in the in vitro AD model compared to the 20 mu M A beta(1-42) treatment group (p < 0.05), whereas Hesperidin had no effect (p > 0.05). Both pre-treatment with Hesperidin and DRB significantly decreased A beta(1-42) levels (p < 0.01), p-Tau (T181) levels (p < 0.05), and the Bax/Bcl-2 ratio (p < 0.05). As a result, our study showed that both Hesperidin and DRB inhibited A beta production by suppressing the amyloidogenic pathway and activating the non-amyloidogenic pathway while also exerting an inhibitory effect on neuronal apoptosis. CK2 may be a potential therapeutic target and could contribute to the pathophysiology of AD. However, these findings should be validated by further studies.