目的 探讨猿猴白血病病毒融合基因包膜糖蛋白(GALV-FMG)诱导白血病HL-60细胞的死亡效应与NF-κB的关系.方法 将HL-60细胞分为pcDNA3.1(+)-GALV-FMG质粒转染(A)组、pcDNA3.1(+)空载体对照(B)组和空白对照(C)组.脂质体转染后,应用乳酸脱氢酶释放实验检测GALV-FMG引起HL-60细胞的死亡效应,免疫荧光和凝胶电迁移检验分析GALV-FMG在诱导HL-60细胞死亡中NF-κB的活性.结果 与B、C组相比,A组细胞中NF-κB的活性受到了明显的抑制,细胞死亡的发生显著增加(P＜0.05).结论 GALV-FMG的表达可诱导HL-60细胞发生死亡;其机制可能与NF-κB的活性抑制有关.%Objective To investigate the relationship between HL-60 cell death induced by gibbon ape leukemia virus fusion gene envelope glycoprotein (GALV-FMG) and NF-kB activity. Methods HL-60 cells were divided into three groups of A[transfected with pcDNA3. l( + )-GALV-FMG],B[transfected with empty pcDNA3.1( + ) vector] and C(blank controls). After lipofectamine transfection, HL-60 cell death induced by GALV-FMG was detected by lactate dehydrogenase release test, and NF-kB activity was analyzed by immunofluorescence and electrophoretic mobility shift assay. Results Compared with groups of B and C, NF-kB activity was significantly inhibited and cell death was remarkably increased in group C(P<0. 05). Conclusion GALV-FMG expression can induce HL-60 cell death, which may be related with inhibition of NF-kB activity.
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