中文摘要：

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-1和Hsp90的基因表达增加而抑制急性白血病细胞株HL-150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。

英文摘要：

Objective To investigate the effect of vascular endothelial growth factor （VEGF） on apoptosis of human acute myeloid leukemia HL-60 cell line and to analyze the functions of the related apoptosis genes including Bcl-2, Mcl-1 and Hsp90. Methods We detected the morphology of HL-60 cells and the apoptosis by single-cell gel electrophoresis（SCGE） and flow cytometry（FCM） ;RT-PCR was used to detect the expression of the apoptosis related genes Bcl-2, Mcl-1 and Hsp90 in mRNA level after 18 hours＇ treating to leukemia cells by VEGF at three concentration by VEGF plus VP16（20 mg/L）, and VP 16（20 mg/L） only. Results The apoptosis of HL-60 cells was inhibited dose dependently by VEGF（2 ug/L, 20 ug/L, 100 ug/L）, and VEGF could decreased the apoptosis induced by Etoposide（VP-16） exposure. The mRNA expression of Bcl-2, Mcl-1 and Hsp90 in HL-60 cells were significantly increased. Conclusions VEGF could inhibit the apoptosis of acute leukemia HL-60 cell by increasing mRNA expression in Bcl-2, Mcl-1 and Hspg0, which may play an important role in the pathogenesis of human acute myeloid leukemia.