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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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    Gut barrier protein levels in serial blood samples from critically ill trauma patients during and after intensive care unit stay
    (Springer Heidelberg, 2023) Donmez-Altuntas, Hamiyet; Ergul, Serap Sahin; Altin-Celik, Pinar; Bulut, Kadir; Eciroglu, Hamiyet; Uzen, Ramazan; Sahin, Gulsah Gunes
    PurposeIn an effort to better manage critically ill patients hospitalised in the intensive care unit (ICU) after experiencing multiple traumas, the present study aimed to assess whether plasma levels of intestinal epithelial cell barrier proteins, including occludin, claudin-1, junctional adhesion molecule (JAM-1), tricellulin and zonulin, could be used as novel biomarkers. Additional potential markers such as intestinal fatty acid-binding protein (I-FABP), d-lactate, lipopolysaccharide (LPS) and citrulline were also evaluated. We also aimed to determine the possible relationships between the clinical, laboratory, and nutritional status of patients and the measured marker levels.MethodsPlasma samples from 29 patients (first, second, fifth and tenth days in the ICU and on days 7, 30 and 60 after hospital discharge) and 23 controls were subjected to commercial enzyme-linked immunosorbent assay (ELISA) testing.ResultsOn first day (admission) and on the second day, plasma I-FABP, d-lactate, citrulline, occludin, claudin-1, tricellulin and zonulin levels were high in trauma patients and positively correlated with lactate, C-reactive protein (CRP), number of days of ICU hospitalisation, Acute Physiology and Chronic Health Evaluation II (APACHE II) score and daily Sequential Organ Failure Assessment (SOFA) scores (P < 0.05-P < 0.01).ConclusionThe results of the present study showed that occludin, claudin-1, tricellulin and zonulin proteins, as well as I-FABP, d-lactate and citrulline, may be used as promising biomarkers for the evaluation of disease severity in critically ill trauma patients, despite the complexity of the analysis of various barrier markers. However, our results should be supported by future studies.
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    Increased oxidative and chromosomal DNA damage in patients with ankylosing spondylitis: its role in pathogenesis
    (Springer-Verlag Italia Srl, 2023) Kiranatlioglu-Firat, Funda; Demir, Huseyin; Cuce, Isa; Altin-Celik, Pinar; Eciroglu, Hamiyet; Bayram, Fahri; Donmez-Altuntas, Hamiyet
    Increased DNA damage has been suggested to contribute to the pathogenesis of chronic inflammatory diseases, but controlled studies are lacking in ankylosing spondylitis (AS). Therefore, we assessed oxidative stress, oxidative DNA damage, chromosomal DNA damage, cell proliferation and cell death in the peripheral blood lymphocytes of patients with AS as well as the possible role of DNA damage in the development of the disease. In total, 25 newly diagnosed AS patients who had not received anti-inflammatory agents and 25 healthy controls were recruited. Oxidative DNA damage was assessed by plasma 8-hydroxy-2 '-deoxyguanosine (8-OHdG) levels, and chromosomal DNA damage was assessed by the cytokinesis-block micronucleus cytome (CBMN-cyt) method. Compared to controls, the micronucleus (MN) frequencies, nucleoplasmic bridge (NPB) frequencies, nuclear bud (NBUD) frequencies, apoptotic cell frequencies, necrotic cell frequencies and plasma 8-OHdG levels were significantly higher in patients with AS (p < 0.001, p < 0.05, p < 0.01, p < 0.001, p < 0.001, and p < 0.001, respectively), and the metaphase cell numbers, binucleated (BN) cell frequencies and nuclear division index (NDI) values were significantly lower in patients with AS (p < 0.01, p < 0.001 and p < 0.001, respectively). Thus, the present findings suggested that oxidative stress, oxidative DNA damage, and chromosomal DNA damage may be involved in the pathogenesis of AS similar to other chronic inflammatory diseases. In addition, the increased plasma 8-OHdG levels, MN frequencies, NPB frequencies and NBUD frequencies in AS patients may reflect an increased cancer risk.
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    Iturin A and Gramicidin A inhibit proliferation, trigger apoptosis, and regulate inflammation in breast cancer cells
    (Elsevier, 2024) Altin-Celik, Pinar; Eken, Ahmet; Derya-Andeden, Muazzez; Eciroglu, Hamiyet; Uzen, Ramazan; Donmez-Altuntas, Hamiyet
    Biosurfactants with antibiotic, antiviral, anti-tumor, and immunomodulatory properties appear to have potential in cancer treatment due to their lack of known toxicities compared with conventional chemotherapy. However, there are few studies on the use of biosurfactants for the treatment of breast cancer. In this study, to develop a new strategy for breast cancer treatment, we evaluated the anti-proliferative, anti-inflammatory, anti-tumor, and apoptotic effects of two different biosurfactants (Iturin A and Gramicidin A) from bacillus in both single and binary combination on two breast cancer cell lines (MDA-MB-231 and MCF-7, which is estrogen receptornegative and positive, respectively). First, the anti-proliferative effects of Iturin A and Gramicidin A, both single and in combination, were explored by MTT assay. Then, the effects of Iturin A and Gramicidin A on inflammatory factors were evaluated using the ELISA method. Apoptosis was assessed using Annexin V-PE/7-AAD and Giemsa staining methods. RT-qPCR analysis was used to evaluate the expressions of several cytokines with anti-tumor and apoptotic properties and the apoptotic BAX and BCL2 genes. Biosurfactants showed antiproliferative and anti-tumor properties by decreasing the viability of MDA-MB-231 and MCF-7 cells depending on concentration and time (p < 0.05-p<0.01). Biosurfactants induced apoptosis by stimulating apoptotic cell death (p < 0.05-p<0.001) and by increasing BAX and decreasing BCL2 gene expression levels (p < 0.05p<0.001) in breast cancer cells. Biosurfactants also regulated the expressions of extracellular and intracellular cytokines (IL-2, IL-6, IL-12, IL12RB2, TGF beta, TNF alpha, VEGF) and chemokines (IL-8, CCL2, CXCL10) in breast cancer cells (p < 0.05-p<0.01). Both single and binary combination applications of Iturin A and Gramicidin A biosurfactants, may potentially treat breast cancer patients, and the in vitro results presented here warrant further in vivo studies.
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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.
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    The increased chromosomal DNA damage in patients with Familial Mediterranean Fever
    (Taylor & Francis Ltd, 2024) Kiraz, Aslihan; Eciroglu, Hamiyet; Altin-Celik, Pinar; Donmez-Altuntas, Hamiyet
    Familial Mediterranean Fever (FMF) is an inherited autoinflammatory disease. In this study, we aimed to assess chromosomal DNA damage and cell proliferation by using cytokinesis-block micronucleus cytome (CBMN-cyt) assay in the peripheral blood lymphocytes of untreated FMF patients carrying M694V and R202Q mutations, which are the most common MEFV gene mutations in Turkish society. The study included 20 untreated FMF patients with M694V and R202Q mutations and 20 healthy individuals of similar age and sex as the control group. Micronucleus (MN), nucleoplasmic bridges (NPBs), and nuclear buds (NBUDs) were scored in the obtained bi-nucleated (BN) cells. Additionally, the nuclear division index (NDI) was calculated using the scores of mononuclear, binuclear, and multinuclear cells. We found that MN and NPBs frequencies in FMF patients were significantly higher than in controls, and number of metaphases was significantly lower (respectively, p < 0.05, p < 0.01, and p < 0.01). However, there was no significant difference in NBUDs frequencies and NDI values between FMF patients and controls (p > 0.05). Our study is the first to evaluate FMF patients' lymphocytes using the CBMN-cyt assay, as no previous research has been found in this respect. Increased MN and NPB frequencies may be useful as biomarkers for chromosomal DNA damage, and may indicate a potential for elevated cancer risk in untreated FMF patients.