WoS İndeksli Yayınlar Koleksiyonu
Permanent URI for this collectionhttps://hdl.handle.net/20.500.14627/6
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Article Citation - WoS: 2Citation - Scopus: 3Biological Activities of Etodolac-Based Hydrazone, Thiazolidinone and Triazole Derivatives on Breast Cancer Cell Lines MCF-7 and MDA-MB(Wiley, 2025) Sevinc, Sevgi Kocyigit; Cikla-Suzgun, Pelin; Tiber, Pinar Mega; Kucukguzel, S. Guniz; Orun, Oya; Güniz Küçükgüzel, Ş.In this study, several etodolac-based hydrazone, thiazolidinone, and triazole derivatives that we synthesized and characterized in our earlier research were tested against the hormone-responsive breast cell line MCF-7 and the triple-negative MDA-MB-231, as well as the murine origin fibroblast cell line L-929, at varying doses for their effects on cell viability and toxicity and for their inhibitory activity on cyclooxygenase-2 (COX-2)/prostaglandin E2 (PGE2) formation. Cell viability and apoptosis tests were utilized to assess the anti-cancer potential of etodolac and its derivatives after the cells were exposed to varied concentrations of synthesized compounds for three different time periods. ELISA and Western blot methods were used to detect protein levels. All synthesized compounds demonstrated higher anti-cancer activity at significantly lower doses compared to etodolac (half-maximal inhibitory concentration [IC50] of 0-50 mu M range in derivatives versus 0.5-1 mM range in etodolac). Except for SGK 242, which had a major toxic effect on all cells, the chemicals SGK 206 and SGK 217 had a twice-less impact on control murine L-929 fibroblasts. Similar to proliferation, low concentrations of SGK 206 and SGK 217 (25-50 mu M) significantly induced apoptosis in breast cancer cells but not in normal cells. Additionally, they inhibited COX-2 protein expression at 50 mu M, and SGK 206 inhibited PGE2 release more effectively than etodolac in cancer cells. The results of this study suggest that, in comparison to a healthy control group, the thiazolidinone derivative SGK 206 and the thiazolidinone derivative SGK 217 are more effective than etodolac when it comes to the breast cancer cell lines MCF-7 and MDA-MB-231. SGK 206 exhibits a low IC50 value, a distinct dose-response relationship, and strong apoptotic effects, particularly on MDA-MB-231 cells.Article Citation - WoS: 1Citation - Scopus: 2Apocynin Exhibits an Ameliorative Effect on Endothelial Dysfunction/ Atherosclerosis-Related Factors in High-Fat Diet-Induced Obesity in Rats(Marmara Univ, Fac Medicine, 2024) Ayci, Nurdan Bulbul; Ertas, Busra; Kaya, Rumeysa Keles; Sevinc, Sevgi Kocyigit; Amuran, Gokce Gullu; Ercan, Feriha; Cetinel, Sule; Keles Kaya, Rumeysa; Bulbul Ayci, Nurdan; Kocyigit Sevinc, SevgiObjective: The aim of this study was to reveal the effect of apocynin (APO) on the factors involved in obesity-related endothelial dysfunction (ED) and atherosclerosis (AS). Materials and Methods: Male Wistar albino rats were divided into control (CNT), high-fat diet (HFD) and HFD+APO groups. HFD and HFD+APO groups were fed HFD for sixteen weeks. APO (25 mg/kg) was administered to the HFD+APO group for the last four weeks. The effects of APO on: AS-related metabolic parameters (triglyceride, total cholesterol, high-density lipoprotein-cholesterol, insulin and leptin), oxidative stress (OS), [ malondialdehyde, glutathione, nicotinamide adenine dinucleotide phosphate (NADPH)oxidase-2, oxidised-low-density lipoprotein (ox-LDL) and 8-hydroxy-2-deoxyguanosine], low-density lipoprotein and ox-LDL uptake potential (activin receptor-like kinase-1 and lectin-like oxidized low-density lipoprotein receptor-1, respectively), tissue inflammation inducible-nitric oxide synthase, nitric oxide), programmed cell death (terminal deoxynucleotidyl-transferase-dUTP-nick-end (alpha-smooth muscle actin), histology and ultrastructure of thoracic aorta were evaluated. Results: In obesity, APO had an ameliorative effect on metabolic parameters, OS, inflammation, ED, programmed cell death and oxLDL uptake potential, but not on foam cell formation and LDL uptake potential. Conclusion: Apocynin may improve ED and AS in obesity by suppressing OS-linked factors involved in the early stage of AS.Article Citation - WoS: 7Effect of Flurbiprofen Derivative (sgk597) on Cell Proliferation and Apoptosis of Breast Cancer Cell Lines(Istanbul Univ, Fac Pharmacy, 2022) Atlihan, Irem; Sevinc, Sevgi Kocyigit; Orun, Oya; Yilmaz, Ozgur; Kucukguzel, S. Guniz; Tiber, Pinar MegaBackground and Aims: The incidence of breast cancer is increasing day by day, especially in women. The search for new drugs against breast cancer is the focus of attention in research. Breast cancer and prostate cancer have remarkable biological similarities. Therefore, the 4-(4-chlorophenyl)-3-(1-(2-fluoro-[1,1'-biphenyl]-4-yl)ethyl)-5-((4-fluorobenzyl)thio)-4H-1,2,4-triazole (SGK597) compound that is suppressing cell proliferation in prostate cancer, was studied in MCF-7 breast can-cer and MCF-10A mammary epithelial cell lines. Methods: The WST-8 method was used to determine cell viability and cytotoxicity of SGK597 in MCF-7 and MCF10-A cell lines. The JC-1 test was applied to determine changes in mitochondrial membrane potential. The protein expression levels of Bax, Bcl-2, and c-PARP associated with apoptosis were determined using Western blot analysis.Results: After 24 and 48 hours of incubation of SGK597, the IC50 values were 28.74 pM and 17.28 pM for MCF-7; 65.9 pM and 50.5 pM for MCF-10A, respectively. Mitochondrial membrane potential showed a tendency toward depolarization in MCF-7 cells as a result of increasing concentration of SGK597, while the same tendency was not seen for MCF-10A. As a result of western blot experiments, no increase in the Bax/Bcl-2 ratio and c-PARP expression level was observed, indicating no apoptosis.Conclusion: It was observed that the compound SGK597 suppressed MCF-7 cell proliferation. These results indicate that SGK597 may be a candidate compound for use as an anticancer agent. Keywords: Apoptosis, breast cancer, flurbiprofen, thioether, triazole