^(60)Co γ射线照射对K562细胞凋亡的影响及其作用机制的研究

STUDY OF THE EFFECT OF ^(60)Co γ RADIATION ON THE APOPTOSIS OF K562 CELLS AND ITS MECHANISM

采用不同剂量的60Coγ射线照射人红细胞系白血病细胞(K562细胞),于照射后不同时间用流式细胞仪检测细胞凋亡率、蛋白免疫印迹法检测凋亡相关蛋白Bcl-2和Bax、流式细胞仪检测细胞周期的变化,以探讨60Coγ射线照射对K562细胞凋亡的影响及其作用机制。结果表明,与正常对照组相比,3和7 Gy剂量组在照后48和72 h,101、5和20 Gy剂量组在照后72 h细胞凋亡率显著升高。2 Gy照射后24 h,照射组的G2/M期阻滞明显(p<0.05),S期细胞比例明显减少(p<0.05),照射组Bcl-2/Bax比例明显比正常对照组降低。以上结果说明,随着照射剂量的增加和时间的延长,细胞凋亡率有随之上升的趋势;γ射线对细胞周期的影响主要是显著的G2/M期阻滞和S期细胞减少;γ射线可能是通过线粒体途径诱导K562细胞凋亡。

To investigate the effect of 7 radiation on the apoptosis of K562 cells and its mechanism, K562 cells were exposed to different doses of ^60Co ganmma radiation （0, 0.5, 1, 3, 7, 10, 15 and 20 Gy, respectively ） and then apoptosis was examined 24, 48 and 72 h after exposure with flow cytometry.Expressions of Bcl-2 and Bax were examined with Western blot and cell cycle was examined with flow cytometry. Results showed that in contrast to the control group, radiation-induced apoptosis ratio for 3 and 7 Gy increased dose group 48 h and 72 h after exposured and for 3, 7, 10, 15 and 20 Gy dose group 72 h after exposure （p 〈0.05） significantly. G2/M phase was delayed and S phase cell ratio decreased in K562 cell cycle when exposed to gamma radiation 24 h after exposure （p 〈 0.05）. The expression of Bax protein increased and the Bcl-2 did＇ t change obviously in the K562 cells when exposed to gamma radiation. The conclusion shows that the apoptosis ratio increased with the increase of irradiation dosage and as the time of apoptosis prolonged, G2/M phase delayed and S phase cell ratio decreased in K562 cell cycle when exposed to gamma radiation. The apoptosis of K562 cells was induced by y radiation via the mitochondrial-mediated pathway.