Özet:

This study was aimed at the study of the cytotoxic, apoptotic and autophysical effects of timokinone on human acute myeloid leucemia. The cytotoxic effects of timokinone were determined by the 3-(4.5-dimetiltiazole2-yl)-2,5-difenyltetrazole-bromide (MTT) test. X-protein (Bax), B-cell lymphoma 2 (Bcl-2), kaspas 3, rapamisine breast target (mTOR), phosfatidylinositol-3-kinase (PI3K) and protein kinase B (AKT) gen expression analyses were carried out with quantitative real-time polymerase chain reaction (qRT-PCR). The software AutoDock Tools 4.2 was used to investigate the potential link of timokinone in the active area of Bax, Bcl-2, Caspas 3, mTOR, ACT and PI3K proteins. Timokinone, in HL-60 cells (human leukemia cell line) 16. It has caused a cytotoxic effect of 35 μM. In all doses administered, Bcl-2 expression was reduced according to control. In cells treated with 10 μM, 15 μM and 25 μM timokinone, a reduction in the expression level of kaspas 3 was observed under control. Timokinone caused a significant decrease in mTOR and PI3K expressions compared to control in all doses, while ACT decreased at a dose of 15 μM. The placement results indicated that timokinone interacted with apoptotic and autofayic proteins through the active area amino acids with hydrophobic interactions and hydrogen bonds. Our findings suggest that timokinone can stimulate autophysics by preventing the PI3K/AKT/mTOR pathway in HL-60 cells and can be a new target for the treatment of acute myeloid leukemia.

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