摘要
目的:探讨小檗胺诱导慢性粒细胞白血病细胞株K562细胞凋亡的机制。方法:体外培养K562细胞株细胞,经8μg/ml小檗胺处理不同时间后用Western blot检测细胞内总NF-κB、核内NF-κB和IκBα、pIκBα、IKKα、A20蛋白表达。结果:随着小檗胺处理时间的延长,细胞内总NF-κB无变化,但核内的NF-κB表达下降,半定量比值从处理前的59.2%,随着作用时间的延长,逐步下降为31.4%,19.7%,4.1%,0%。同时出现pIκBα、IKKα表达下调,A20表达增高。结论:小檗胺通过NF-κB途径诱导慢性粒细胞白血病细胞株K562细胞凋亡的机制,可能涉及抑制NF-κB的核转位和转激活,推测其作用与小檗胺降低K562细胞bcr-abl基因的表达有关。
Objective： To investigate the mechanism related to the inhibition of leukemia K562 cells by berbamine. Methods： After K562 cells were treated with 8 μg/ml berbamine, the expression levels of NF-k,IkBα,pIkBa, IKKα, A20 were determined by Western blot. Results ： With the exposure time extending, the total NF-kB showed no significant changes, but NF-kB expression in nucleus was decreased dramatically after treated with berbamine for 24 h. The ratio of nucleus NF-kB/histone H1 was decreased from 59.2% ,gradually to 31.4%, 19.7% ,4.1% ,and 0%. At the same time,the expression of A20 was increased,while the expression of pIkBa,IKKa was down-regulated. Conclusion： Berbamine may induce K562 cell apoptosis through NF-kB pathway. Down-regulation of NF-kB and bcr-abl gene expression might be involved in cell apoptosis.
出处
《浙江大学学报（医学版）》
CAS
CSCD
北大核心
2009年第4期387-391,共5页
Journal of Zhejiang University(Medical Sciences)
