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目的探讨血管内皮生长因子(VEGF)在体外对人急性白血病细胞株HL-60的凋亡及相关基因B细胞白血病-2(Bcl-2)、髓样细胞白血病-1(Mcl-1)和热休克蛋白90(Hsp90)表达的影响。方法采用彗星电泳法和流式细胞术等检测经VEGF处理后HL-60细胞株的细胞凋亡率,并观察VEGF对抗细胞凋亡诱导剂鬼臼乙叉(VP16)的效应。采用RT-PCR方法从mRNA水平分别检测该细胞株的Bcl-2、Mcl-1和Hsp90等基因的表达水平。结果三种浓度VEGF(2ug/L、20ug/L、100ug/L)处理的HL-60细胞株的凋亡明显受到抑制,并且VEGF可以对抗VP16诱导的细胞凋亡效应。2ug/L的VEGF处理HL-60细胞株18h后其细胞内的凋亡相关基因Bcl-2、Mcl-1和Hsp90的mRNA表达明显增加。结论VEGF可能通过提高Bcl-2、Mcl-l和Hsp90的基因表达增加而抑制急性白血病细胞株HL-60的凋亡;VECF可以抑制人急性白血病细胞的凋亡可能是白血病的发病机制之一。
Objective To investigate the effects of vascular endothelial growth factor (VEGF) on the apoptosis of human acute leukemia cell line HL-60 and the expression of related genes Bcl-2, Mcl-1 and heat Impact of shock protein 90 (Hsp90) expression. Methods The apoptotic rates of HL-60 cells treated with VEGF were detected by comet assay and flow cytometry. The effect of VEGF on the anti-apoptosis inducer VP16 was also observed. The expression levels of Bcl-2, Mcl-1 and Hsp90 genes in this cell line were detected by RT-PCR from mRNA level. Results The apoptosis of HL-60 cells treated with three concentrations of VEGF (2ug / L, 20ug / L, 100ug / L) was significantly inhibited and VEGF could antagonize the VP16-induced apoptosis. The expression of Bcl-2, Mcl-1 and Hsp90 mRNA in HL-60 cells treated with 2ug / L VEGF for 18h increased significantly. Conclusion VEGF may inhibit the apoptosis of acute leukemia cell line HL-60 by increasing the gene expression of Bcl-2, Mcl-1 and Hsp90. VECF may inhibit the apoptosis of human acute leukemia cells and may be one of the pathogenesis of leukemia.