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Study on Apoptosis of Human promyelocytic leukemia HL-60 Cells Induced by Fucosterol via Death Receptor Pathway

机译:病毒甾醇通过死亡受体途径诱导的人幼胞细胞白血病HL-60细胞凋亡的研究

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The purpose of this study is to investigate the effect of fucosterol on the induction of apoptosis and the molecular mechanism involved in Human promyelocytic leukemia HL-60 Cells. HL-60 Cells were treated with different concentrations of fucosterol at different time. MTT method was used to study fucosterol anti-tumor activity. Morphology observation was performed to determine the effects of fucosterol on apoptosis of HL-60 cells. Flow cytometry (FCM) was used to detect the cell cycle. Laser scanning confocal microscope (LSCM) was used to analyze the expressions of Fas, FasL, Fadd and Caspase-8. Caspase activity kits were used to determine the activity of Caspase-8 and Caspase -3. The results showed fucosterol could inhibit the growth of HL-60 cells, and the apoptosis morphology for 48 h treatment was obvious, which showed cell protuberance, cytoplasm concentrated and apoptotic body. Fucosterol treatment for 24 h increased the protein expression of Fas, FasL, Fadd and Caspase-8. It also showed that the activity of Caspase-3 and Caspase-8 has increased significantly. In conclusion, Fucosterol could induce HL-60 cells apoptosis via death receptor pathway.
机译:本研究的目的是探讨FucosterolOl对人幼儿细胞白血病HL-60细胞诱导和分子机制的影响。在不同时间用不同浓度的Fucosterol治疗HL-60细胞。 MTT方法用于研究Fucosterolol抗肿瘤活性。进行形态学观察,以确定Fucoster OL对HL-60细胞凋亡的影响。流式细胞术(FCM)用于检测细胞周期。激光扫描共聚焦显微镜(LSCM)用于分析Fas,FasL,FADD和Caspase-8的表达。用于确定Caspase-8和Caspase -3的活性的Caspase活性试剂盒。结果表明,Fucosterol可以抑制HL-60细胞的生长,48小时治疗的细胞凋亡形态明显,其显示细胞突出,细胞质浓缩和凋亡体。 FUCOSTEROL治疗24小时增加FAS,FASL,FADD和Caspase-8的蛋白质表达。它还表明,Caspase-3和Caspase-8的活性显着增加。总之,Fucosterol可以通过死亡受体途径诱导HL-60细胞凋亡。

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