电离辐射诱发HL-60细胞凋亡及Bcl-2基因对细胞凋亡的影响

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本实验采用 60 Coγ射线 (剂量分别为 0、2、4、6、8、10 Gy)照射人早幼粒白血病 HL- 60细胞 ,研究了辐射诱发的细胞调亡 ,并对 HL- 60细胞和转染了反义 Bcl- 2基因的 HL - 60细胞 ( HL- 60 as Bcl- 2 )的凋亡情况进行了比较。结果表明 ,60 Coγ射线照射可抑制两种细胞的增殖 ,并可诱导细胞凋亡 ,细胞调亡率与受照剂量呈正相关 ,随照后时间的延长细胞凋亡率也逐渐增加 ;比较照后不同时间的凋亡率 ,照后 2 4 h和4 8h,各剂量点 HL - 60 as Bcl- 2细胞凋亡率均明显高于同剂量 HL- 60细胞 ,而照后 72、96和 12 0 h,同剂量点两种细胞凋亡率未见明显差异。 In this study, 60Co γ-ray (doses 0, 2, 4, 6, 8, 10 Gy) were irradiated on human promyelocytic leukemia HL-60 cells to study the radiation-induced apoptosis. HL- The apoptosis of HL-60 cells transfected with antisense Bcl-2 gene (HL-60 as Bcl-2) was compared. The results showed that 60 Co γ-ray irradiation could inhibit the proliferation of both cells and induce apoptosis. The apoptosis rate was positively correlated with the dose of irradiation, and the apoptosis rate increased with the increase of irradiation time. The apoptotic rates of HL - 60 as Bcl - 2 cells at different dose of 24 h and 48 h after irradiation were significantly higher than those of the same dose of HL - 60 cells at different time points, while 72, 96 and 120 h, the same dose point two kinds of cell apoptosis rate no significant difference.
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