摘要
目的:探讨核因子κB在X射线电离辐射诱导HepG2细胞凋亡中的作用。方法:实验于2004-02/2005-03在南方医科大学南方医院完成。将HepG2细胞分3组:对照组不加任何处理因素;辐射组单纯X射线电离辐射6Gy;核转录因子κB抑制剂组是指在照射前30min用20μmol/L的lactacystin预处理细胞,然后按照同样的辐射条件进行X射线照射。流式细胞仪检测细胞凋亡率,免疫电泳迁移率改变分析法检测细胞内核因子κB的激活,应用SPSS10.0软件包行多组均数间方差分析。结果:对照组、辐射组、核转录因子κB抑制剂组的细胞凋亡率分别是1.73%,20.90%,35.23%。对照组的核因子κB微弱激活,辐射组明显激活,核转录因子κB抑制剂组的活性较辐射组减弱,与对照组相似。结论:辐射可以引起HepG2细胞凋亡,并诱导了核因子κB的激活,且可能在X射线辐射诱导HepG2细胞凋亡中发挥抗凋亡作用。
AIM： To investigate the effect of nuclear factor KB （NF-κB） on apoptosis of HepG2 cells induced by X-ray ionization radiation. METHODS： The experiment was conducted at the Nanfang Hospital, Nanfang Medical University from February 2004 to March 2005. The HepG2 cells were divided into three groups： Those in the control group were without any disposal. Those in the radiation group were with pure X- ray ionization radiation 6Gy and those in the NF-KB inhibitor group were predisposed with 20 μmol/L lactacystin 30 minutes before irradiation, and then given X-ray irradiation according to the same radiation condition. Apoptosis rates of cells were estimated by flow cytometry. The activation of NF-KB in HepG2 cells was evaluated by immunoelectrophoretic mobility shift assay （EMSA）. Analysis of variance of means in multiple groups was conducted with SPSS 10.0 software.
RESULTS： Apoptosis rates of control group, radiation group and NF-κB inhibitor group were 1.73%,20.90% and 35.23%, respectively. NF-κB was activated weakly or feebly in the control group. Those in the radiation group were activated significantly. The activation in the NF-κB inhibitor group became weak as compared with the radiation group, and similar to the control group. CONCLUSION： Radiation can induce the apoptosis of HepG2, the activation of NF-κB and may play an anti-apoptosis role in HepG2 cells induced by X-ray radiation.
出处
《中国临床康复》
CSCD
北大核心
2005年第43期75-77,共3页
Chinese Journal of Clinical Rehabilitation
