TNF-α,G-CSF调节CD3AK细胞诱导的HL-60凋亡

TNF-α, G-CSF Regulation of HL-60 Cells' Apoptosis Inducing by CD3AK Cells

目的 :探讨肿瘤坏死因子α(TNF α) ,粒细胞集落刺激因子 (G CSF)对CD3AK细胞诱导HL 6 0细胞凋亡的影响。方法 :用细胞形态学观察 ,DNA琼脂糖电泳 ,原位末端标记法分别检测HL 6 0自然凋亡率、CD3AK细胞诱导的HL 6 0凋亡率、TNF α和CD3AK诱导的HL 6 0凋亡率、G CSF和CD3AK诱导的HL 6 0凋亡率。结果 :HL 6 0细胞自然凋亡率 (4.6 0± 2 .17) % ;CD3AK细胞诱导HL 6 0细胞凋亡率 (2 7.38± 4 .91) % ;TNF α和CD3AK诱导的HL 6 0凋亡率 (33.0 9± 5 .2 2 ) % ;G CSF和CD3AK(7.35± 2 .2 6 ) % (F =96 .80 ,P <0 .0 1)。结论 :TNF α加强CD3AK细胞诱导的HL 6 0凋亡 ,G CSF抑制CD3AK诱导的HL 6

Objective: To study the effect of TNF α, G CSF on HL 60 cells' apoptosis induced by CD3AK. Methods: Apoptosis was detected by TUNEL technique, cell morphology and DNA agarose gel electrophoresis. The percentage of HL 60 cells apoptosis which were occurrence naturally, was induced by CD3AK, by both CD3AK and TNF α, and by both CD3AK and G CSF. Results: The percentage of HL 60 cells' apoptosis was (4.60±2.17)%, (27.38±4.91)%, (33.09±5.22)%, (7.35±2.26)%, respectively(F=96.80, P<0.01). Conclusion: TNF α helps HL 60 cells' apoptosis induced by CD3AK, G CSF inhibited HL 60 cells' apoptosis induced by CD3AK.