TR Dizin İndeksli Yayınlar Koleksiyonu / TR Dizin Indexed Publications Collection
Permanent URI for this collectionhttps://hdl.handle.net/20.500.14365/4
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Article Aconitine Impedes Cell Motility in Mda-Mb Breast Cancer Cells(Dokuz Eylul Univ Inst Health Sciences, 2024-09-30) Keles, Didem; Sipahi, Murat; Surer, Seniz Inanc; Oktay, GulgunPurpose: Aconitine, a potent alkaloid from Aconitum plants, has shown promising anticancer properties. The aim of the study is to investigate the effects of aconitine on lateral migration, and matrix metalloproteinase (MMP) activity in MDA-MB-231 triple-negative breast cancer cells. Material and Methods: A WST-1 viability assay was conducted to determine the effect of aconitine on the viability of MDA-MB-231 cells. Following treatment with non-cytotoxic doses of aconitine, lateral migration was evaluated through wound healing assays. Additionally, gelatin zymography was conducted to analyze MMP-2 and MMP-9 activity and secretion levels. Results: Aconitine concentrations up to 200 mu M did not significantly affect cell viability for up to 72 hours, whereas higher doses (400-600 mu M) reduced viability in a time-dependent manner. Aconitine at 200 mu M showed a trend towards decreased lateral motility, with a significant reduction at 9 hours post-treatment. Gelatin zymography revealed no alterations in MMP-2 and MMP-9 activity or secretion levels following aconitine treatment. Conclusion: Aconitine demonstrates limited efficacy in modulating the migratory capacity of MDA-MB231 cells and does not affect gelatinase activity. Further investigation into underlying mechanisms is necessary, potentially leading to novel therapeutic strategies for triple-negative breast cancer.Article Citation - WoS: 3Citation - Scopus: 3Effects of Kynurenic Acid and Choline on Lipopolysaccharide-Induced Cyclooxygenase Pathway(Walter De Gruyter Gmbh, 2023-06-01) Barış, Elif; Şimşek, Oguzhan; Uysal Yoca, Özge; Demir, Ayşe Banu; Tosun, Metiner; Yoca, Ozge UysalObjectives: Inflammation can be endogenously modulated by the cholinergic anti-inflammatory pathway via calcium (Ca2+)-permeable alpha-7 nicotinic acetylcholine receptor (a7nAChR) ion channel expressed in immune cells. a7nAChR agonist choline and tryptophan metabolite kynurenic acid (KYNA) produces immunomodulatory effects. This study aimed to determine the effects of the choline and KYNA on the lipopolysaccharide (LPS)-induced cyclooxygenase (COX)-2 pathway.Methods: In vitro inflammation model was produced via LPS administration in macrophage cells. To determine the effective concentrations, choline and KYNA were applied with increasing concentrations and LPS-induced inflammatory parameters investigated. The involvement of nAChR mediated effects was investigated with the use of non-selective nAChR and selective a7nAChR antagonists. The effects of choline and KYNA on COX-2 enzyme, PGE(2), TNFa, NF-?B and intracellular Ca2+ levels were analyzed.Results: LPS-induced COX-2 expression, PGE(2) TNFa and NF-?B levels were decreased with choline treatment while intracellular calcium levels via a7nAChRs increased. KYNA also showed an anti-inflammatory effect on the same parameters. Additionally, KYNA administration increased the effectiveness of choline on these inflammatory mediators.Conclusions: Our data suggest a possible interaction between the kynurenine pathway and the cholinergic system on the modulation of LPS-induced inflammatory response in macrophages.Article Can Spesific Biomarkers Be Used To Enlighten the Major Mechanisms of Acute High Dose Diclofenac Sodium-Related Nephrotoxicity?(Galenos Publ House, 2022-06-01) Dogruyol, Sinem; Akbas, Ilker; Kocak, Abdullah Osman; Aygormez, Serpil; Leylek, Habip Emrah; Gur, Sultan Tuna Akgol; Ertener, Ozge; Cokbankir, OzgeAim: The aim of this study was to examine the basic mechanisms that play a role in the acute nephrotoxicity caused by diclofenac sodium. Materials and Methods: Only water was given to the control group; however, the diclofenac sodium group was group intoxicated by giving water-soluble, 240 mg/kg, oral single dose diclofenac sodium. After 24 hours, all animals were sacrificed and histopathological analyzes were performed. The levels of spesific biomarkers [vascular endothelial growth factor (VEGF), nuclear factor-kappa B (NF-kappa B), matrix metalloproteinase-9 (MMP-9), metalloproteinase tissue inhibitor-1 (TIMP-1) and carcinoembryonic antigen (CEA)] that may be related to the nephrotoxicity mechanism were evaluated. Results: As a result of biochemical analysis, we found that VEGF, TIMP-1, NF-kappa B and CEA levels were significantly higher and MMP-9 levels were significantly lower in diclofenac sodium group compared to control group. Nephrotoxicity related histopathological changes were observed in the sections of diclofenac sodium group. Conclusion: This study has shown that the biomarkers we evaluated in the diclofenac sodium-induced acute high-dose intoxication model we created can help us to identify the nephrotoxicity and to explain the nephrotoxicity mechanism with the three main steps (the hemodynamicrelated pathway, the inflammation-related pathway, and the oxidative stress-related pathway). With a simple version of this panel adapted to emergency departments, we may be able to diagnose diclofenac sodium-related nephrotoxicity.Article Citation - WoS: 3Citation - Scopus: 6Effects of Bevacizumab Administration on the Hypoxia- Induced Pulmonary Hypertension Rat Model(Tubitak Scientific & Technical Research Council Turkey, 2021-10-21) Demir, Canan; Karaman, Meral; Ucan, Eyup Sabri; Gokmen, Ali Necati; Gurel, Duygu; Coker, Sadiye Canan; Adali, Yasemen; Yilmaz, Osman; Gokmen, Necati; Coker, CananBackground/aim: Bevacizumab is a chemotherapeutic drug, which selectively binds to vascular endothelial growth factor (VEGF) and mainly inhibits angiogenesis and neovascularization. We aimed to study the possible effects of bevacizumab on right ventricular pressure (RVP), right ventricular hypertrophy, and VEGF, in hypoxia -induced pulmonary hypertension (PH) rat model. Materials and methods: 24 adult Wistar Albino rats were randomly divided into four groups: control group -saline; Bevacizumab Group; PH Group; PH + Bevacizumab Group. In hypoxia -induced model, 10% oxygen and 90% nitrogen were applied in a plexiglas box for eight days to PH Group and PH + Bevacizumab Group. On day eight, RVPs were measured directly from the heart, and then animals were sacrificed. Heart and lung tissues were examined, and Fulton index was measured. Results: RVP, Fulton index, and tissue VEGF scores were significantly lower in PH + Bevacizumab group than PH group: median (ranges), RVP, mmHg, 37.8 (33.0-39.0) and 32.3 (28.0-35.0), p: 0.01; Fulton index: 0.30 (0.29-0.33) and 0.25 (0.24-0.26), p: 0.003; tissue VEGF scores: 5.1 (4.8-5.3) and 4.0 (3.8 4.1), p: 0.004, respectively. Conclusion: Bevacizumab, which is indeed an antineoplastic agent, might have a favorable effect on hypoxia -induced pulmonary hypertension.