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    Cytotoxic and genotoxic effects of nateglinide on human ovarian, prostate, and colon cancer cell lines
    (2023) Öz, Samet; Şekerci, Güldeniz; Yüksel, Furkan; Tekin, Suat
    Aim: Nateglinide, an oral anti-diabetic medication used to treat type 2 diabetes, activates ATP-dependent potassium channels in pancreatic beta cells and induces insulin secretion. Numerous antidiabetic medicines, particularly metformin, are known to drastically reduce the viability of cancer cells. This study examined the effects of nateglinide on the DNA and viability of human ovarian (A2780), prostate (LNCaP), and colon (Caco-2) cancer cells. Materials and Methods: Initially in the study, 1, 10, 100, and 1000 µM doses of nateglinide were administered for 24 hours to A2780, LNCaP, and Caco-2 cells. The 3-(4,5- dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) test was used to measure cell viability. Using Graphpad Prism 8, the inhibitory logarithmic concentration values (LogIC50) of nateglinide in A2780, LNCaP, and Caco-2 cells were computed based on the results of the MTT experiment. These doses were applied to A2780, LNCaP, and Caco-2 cells for the Comet assay. The Bonferroni-corrected Mann–Whitney U test was used to compare groups, and a value of p<0.05 was considered statistically significant. Results: In A2780 and LNCaP cell lines, only 1000 µM nateglinide concentration de creased cell viability (p<0.05), whereas in Caco-2 cells, all concentrations except 1 µM reduced cell viability (p<0.05). The Comet assay indicated that nateglinide produced DNA damage by increasing the tail lengths and tail moments of A2780, LNCaP, and Caco-2 cells (p<0.05) and reducing the head diameters (p<0.05). Conclusion: According to the findings of this study, nateglinide has cytotoxic effects on human ovarian, prostate and colon cancer cell lines and may possess anticancer properties.
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    İn Vitro ve İn Vivo olarak oluşturulan deneysel diyabet modelinde Saksagliptin'in etkilerinin araştırılması
    (İnönü Üniversitesi, 2025) Öz, Samet; Tekin, Suat
    Amaç: Diyabet, insülin metabolizmasındaki bozulmalar sonucu gelişen kronik bir hastalıktır ve uzun süreli hiperglisemi diyabetik nöropatiye (DN) yol açmaktadır. Bu çalışmada, bir DPP-4 inhibitörü olan Saksagliptin'in (Sax) DN modellerindeki etkinliği değerlendirilmiştir. Materyal ve Metot: Çalışmada 40 adet Balb-c ırkı erkek fare kontrol, DN, DN+Sax-2 ve DN+Sax-10 olmak üzere 4 gruba ayrıldı (n=10). Kontrol dışındaki gruplara intraperitonal olarak tek doz streptozotosin (150mg/kg) enjekte edildi ve 21 gün süresince DN modeli oluşması için beklenildi. Kontrol grubuna bir uygulama yapılmazken, DN grubuna serum fizyolojik, DN+Sax-2 ve DN+Sax-10 gruplarına ise sırasıyla 2 ve 10mg/kg dozlarında Sax, oral gavaj yoluyla 15 gün süresince uygulandı. Bu süre boyunca farelerde nosiseptif davranış testleri (hot plate, tail flick, von Frey) gerçekleştirildi. 15.gün fareler dekapite edilerek pankreas ve kan dokuları toplandı. Çalışmanın in vitro basamağında ise 1-2 günlük Wistar Albino cinsi sıçanlardan dorsal kök gangliyonları (DKG) 24 saat yüksek glikoza maruz bırakıldı ve Sax'ın hücre canlılığına etkisi ile kullandığı hücresel yolak belirlendi. Elde edilen sonuçlar SPSS paket programında uygun istatistiksel yöntemler kullanılarak analiz edildi ve p<0.05 anlamlı kabul edildi. Bulgular: Sax'ın farelerde DN grubuna kıyasla ağrı eşiğini arttırdığı (p<0.05), antioksidan ve antiinflamatuar etkiler gösterdiği (p<0.05) ve pankreasın histolojik bütünlüğünü korumaya yardımcı olduğu belirlendi (p<0.05). Ayrıca Sax'ın DKG'de fosfoinositid-3 kinaz yolağını kullanarak hücre canlılığını arttırdığı tespit edildi (p<0.05). Sonuç: STZ kaynaklı diyabetik nöropatide, DPP-4 enzim inhibitörü olan Sax, terapötik potansiyel etkiler göstermektedir. Anahtar Kelimeler: Diyabet, DKG, Nöropatik Ağrı, Saksagliptin
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    INVESTIGATION OF THE CYTOTOXIC AND GENOTOXIC EFFECTS OF PAROXETINE ON HUMAN OVARIAN, PROSTATE AND COLON CANCER CELL LINES
    (Inonu University, 2026) Öz, Samet; Bahar, Mehmet Refik; Özkaya, Semiha Nur; Tekin, Suat
    Cancer is a major public health problem due to uncontrolled cell proliferation, invasion of sur-rounding tissues, and its high prevalence and mortality rates. Despite current treatment strat-egies, the poor prognosis in many cancer types necessitates the exploration of new pharma-cological approaches. In this study, we aimed to evaluate the cytotoxic and genotoxic effects of paroxetine, a potent selective serotonin reuptake inhibitor (SSRI), in human ovarian (A2780), prostate (LNCaP), and colon (Caco-2) cancer cell lines in vitro. A2780, LNCaP, and Caco-2 cells were cultured in appropriate media and treated for 24 hours with paroxetine at concentrations of 1, 10, 100, and 1000 µM. Cell viability was determined using the 3-(4,5-dimethylthiazol-2-yl)-di-phenyltetrazolium bromide (MTT) assay, and the inhibitory concentration was calculated using GraphPad Prism 8 software. DNA damage was assessed using the comet assay. Statistical analyses were performed using IBM SPSS Statistics 24.0 (Windows); p < 0.05 was considered statisti-cally significant. Paroxetine significantly reduced cell viability in A2780 cells at all concentrations except 1 µM, and in LNCaP and Caco-2 cells at 100 and 1000 µM (p < 0.05). Comet assay results demonstrated that paroxetine significantly increased tail length, tail intensity, and olive tail intensity, and decreased head length and head intensity in all cell lines (p < 0.05). Our findings indicate that paroxetine exerts both cytotoxic and genotoxic effects on various cancer cell lines in vitro. These results suggest potential roles of SSRIs in cancer biology beyond their established psychiatric applications. © 2026 The Author(s).