摘要
目的:探讨bcl-2和bax在三氧化二砷(arsenic trioxide,As2O3)诱导HL-60细胞凋亡过程中的变化。方法:7.5μmol/L的As2O3作用HL-60细胞12、24 h,RT-PCR和Western-blot分别检测bcl-2和bax基因mRNA表达及相应的蛋白表达变化。结果:7.5μmol/L的As2O3作用HL-60细胞12、24 h后,bcl-2 mRNA相对表达分别为(65.02±4.69)%、(40.70±3.94)%,baxmRNA相对表达分别为(46.71±4.26)%、(95.65±5.57)%,Western-blot检测bcl-2蛋白相对表达分别为(56.34±6.45)%、(42.01±3.01)%,bax蛋白质表达分别是(50.65±4.50)%、(66.78±5.05)%,对照组与实验组差异均有统计学意义(P<0.01)。结论:As2O3诱导HL-60细胞凋亡过程中,下调bcl-2 mRNA和蛋白质表达,同时上调bax mRNA和蛋白质表达,可能是As2O3诱导细胞凋亡信号传导通路之一。
Objective：To investigate the alteration of bcl-2 and bax experssion in apoptosis of HL-60 cells induced by As2 03 （arsenic trioxide,ATO）. Methods： HL-60 cells were treated with 7.5umol/L As2O3 for 12 and 24 hours, the expressions of bcl-2 and bax mRNA were examined by semi-quantitative RT-PCR, and the activities of bcl-2 and bax protein were determined by Western blot. Results：Treated with 7.5 umol/L As2O3 for 12 and 24h, the relative expressions of bcl-2 mRNA in HL-60 cells were （65.02 ± 4.69 ） % and （40.70 ± 3.94 ） %, and the bax were （46.71 ± 4.26 ） % and （ 95.65 ± 5.57 ） % , respectively. Western blot indicated that the ratio of bcl-2 protein were （ 56.34 ± 6.45 ） % and （42.01± 3.01 ） %, and the bax were （50.65 ± 4.50 ） % and （ 66.78 ± 5.05 ） %, respectively. There was significant difference between control group and experience group（ P 〈0.01 ）. Condusions：As2O3 could downregulate the expression of bcl-2 mRNA and protein, and the same time up-regulate the expression bax mRNA and protein in apoptosis of HL-60 cells. It may be one of signal transduetion in apoptosis of HL-60 cells induced by As2O3.
出处
《蚌埠医学院学报》
CAS
2009年第1期9-11,共3页
Journal of Bengbu Medical College
基金
安徽省教育厅自然科学研究资助项目(2004kj278)
