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SeO2诱导白血病细胞凋亡及对凋亡相关基因Bcl-2和p53表达调控的影响
引用本文:王晓华,魏亚明,白海,欧剑锋,路继红,郑荣梁.SeO2诱导白血病细胞凋亡及对凋亡相关基因Bcl-2和p53表达调控的影响[J].第一军医大学学报,2004,24(10):1160-1163.
作者姓名:王晓华  魏亚明  白海  欧剑锋  路继红  郑荣梁
作者单位:[1]广州医学院生物化学与分子生物学教研室,广东广州510182 [2]南方医科大学南方医院血液科,广东广州510515 [3]兰州军区总医院血液病研究所,甘肃兰州730050 [4]兰州大学生命科学院,甘肃兰州730000
摘    要:目的:研究SeO2对急性早幼粒细胞白血病细胞株NB4、红白血病细胞K562、急性粒细胞白血病细胞株HL-60的增生、凋亡及Bcl-2和p53表达水平的影响。方法:采用流式细胞术测定细胞的凋亡率及Bcl-2和p53的表达。结果:10和30mmol/L SeO2能抑制3种细胞增生。30mmol/L SeO2作用48h能使54.0%的NB4细胞、46.5%的K562细胞和49.6%的HL-60细胞发生凋亡;能使NB4和K562细胞Bcl-2表达显著下降、促进p53的表达。结论:SeO2对3种白血病细胞均有诱导凋亡作用,在凋亡过程中涉及了细胞内凋亡相关基因Bcl-2和p53表达和调控。

关 键 词:硒化合物  凋亡  基因  bcl-2  基因,p53  K562细胞  HL-60细胞  NB4细胞

Apoptosis and regulation of expressions of apoptosis-related gene Bcl-2 and p53 induced by selenium dioxide in three leukemia cell lines]
Xiao-hua Wang,Ya-ming Wei,Hai Bai,Jian-feng Ou,Ji-hong Lu,Rong-liang Zheng.Apoptosis and regulation of expressions of apoptosis-related gene Bcl-2 and p53 induced by selenium dioxide in three leukemia cell lines][J].Journal of First Military Medical University,2004,24(10):1160-1163.
Authors:Xiao-hua Wang  Ya-ming Wei  Hai Bai  Jian-feng Ou  Ji-hong Lu  Rong-liang Zheng
Institution:Department of Biochemistry and Molecular Biology, Guangzhou Medical College, Guangzhou 510182, China. xh_wang2631@sina.com
Abstract:OBJECTIVE: To investigate the mechanisms underlying the effect of selenium dioxide (SeO(2)) on the proliferation, apoptosis, and apoptosis-related gene expressions of Bcl-2 and p53 in 3 leukemia cell lines NB4, K562 and HL-60. METHODS: The three leukemia cell lines were treated with 3, 10 and 30 mmol/L SeO(2) and apoptosis detected by flow cytometry and analysis of p53 and Bcl-2 expressions. RESULTS: SeO(2) at 10 and 30 mmol/L could inhibit the proliferation of three leukemia cell lines. SeO(2) treatment at 30 mmol/L for 48 h induced an apoptosis rate of 54.0 %, 46.5 %, 49.6 % in NB4, K562, and HL-60 cells respectively, and down-regulated Bcl-2 expression in NB4 and K562 but not in HL-60 cells. CONCLUSION: SeO(2) can induce apoptosis in NB4, K562 and HL-60 leukemia cells, involving the down-regulation of Bcl-2 and up-regulation of p53.
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