Yazar "Ata, Hayrettin" seçeneğine göre listele
Listeleniyor 1 - 2 / 2
Sayfa Başına Sonuç
Sıralama seçenekleri
Öğe Role of epigallocatechin gallate on in vitro model of methylglyoxal-induced amyloidogenesis(BRNSS Publication Hub, 2016) Kucukgul, Altug; Işgör, Mehmet Mustafa; Cellat, Mustafa; Ata, HayrettinIntroduction: The study aimed to investigate the potential effects of epigallocatechin gallate (EG) on the reflux of methylglyoxal (MG)-induced amyloidogenesis in human glioblastoma (U87) cells. Materials and Methods: The effective concentrations of MG and EG were investigated via Trypan blue test. Glyoxalase-1 (GLO-1), ?-amyloid precursor protein (?APP), and Caspase 3 (Cas 3) expression levels were determined by quantitative real-time polymerase chain reaction and intracellular glutathione (GSH) contents of cells were measured. Results: MG at 250 ?M reduced viable cells by 33.4% as compared to control group. However, 5 ?M EG pre-treatment before MG prevented 22.4% of the cell loss caused by MG (P ? 0.05). MG stimulated ?APP and Caspase 3 levels by 4.13- and 3.46-fold; however, EG pre-treatment inhibited these increases by 1.76 and 3.09, respectively. In addition, EG pre-treatment increased GLO-1 levels by 3.71-fold and GSH levels by 2.30-fold according to MG group. Conclusion: EG demonstrated protective effect against cell death on U87 cells by suppressing amyloidogenic factors and apoptotic stimuli induced by MG.Öğe Role of Epigallocatechin Gallate on In Vitro Model of Methylglyoxal-induced Amyloidogenesis(Asian Journal Pharmaceutics, 2016) Kucukgul, Altug; Isgor, Mehmet Mustafa; Cellat, Mustafa; Ata, HayrettinIntroduction: The study aimed to investigate the potential effects of epigallocatechin gallate (EG) on the reflux of methylglyoxal (MG)-induced amyloidogenesis in human glioblastoma (U87) cells. Materials and Methods: The effective concentrations of MG and EG were investigated via Trypan blue test. Glyoxalase-1 (GLO-1), beta-amyloid precursor protein (beta APP), and Caspase 3 (Cas 3) expression levels were determined by quantitative real-time polymerase chain reaction and intracellular glutathione (GSH) contents of cells were measured. Results: MG at 250 mu M reduced viable cells by 33.4% as compared to control group. However, 5 mu M EG pre-treatment before MG prevented 22.4% of the cell loss caused by MG (P <= 0.05). MG stimulated beta APP and Caspase 3 levels by 4.13- and 3.46-fold; however, EG pre-treatment inhibited these increases by 1.76 and 3.09, respectively. In addition, EG pre-treatment increased GLO-1 levels by 3.71-fold and GSH levels by 2.30-fold according to MG group. Conclusion: EG demonstrated protective effect against cell death on U87 cells by suppressing amyloidogenic factors and apoptotic stimuli induced by MG.