超声诱导K562细胞凋亡机制的研究  

Mechanisms of K562 Cells Apoptosis Induced by Ultrasound

作　　者：何明生[1] 曹红花[1] 朱念麟[2] 刘鲲[1] 

机构地区：[1]云南省第一人民医院血液科,昆明市650032 [2]云南大学物理系

出　　处：《中国超声医学杂志》2006年第10期724-726,共3页Chinese Journal of Ultrasound in Medicine

基　　金：云南省自然科学基金资助项目(No.2001C0010R)

摘　　要：目的本实验探讨超声体外诱导K562细胞凋亡的影响及其机制。方法频率为1.8MHz的超声波辐照正常外周血单核细胞和体外培养的K562细胞,辐照后用光学显微镜观察凋亡细胞形态学改变、流式细胞仪检测原位末端脱氧核苷酸转移酶(TUNEL)和p53、bcl-2、caspase-3、Fas、FasL蛋白表达水平。结果电压为10mV超声辐照细胞10min后12h和24h,光学显微镜下可见凋亡小体形成等典型形态学改变,K562细胞凋亡率及p53、caspase-3、Fas、FasL蛋白表达水平分别显著高于对照组(P<0.001);而bcl-2蛋白表达水平明显低于对照组(P<0.001)。结论超声可以诱导K562细胞凋亡,其机制可能与p53、caspase-3、Fas、FasL蛋白表达增高及bcl-2蛋白表达降低有关。Objective The effect and potential mechanisms of K562 apoptosis induced by ultrasound were investigated in our study. Methods Normal mononuclear cells and K562 cells were treated with ultrasound at a frequency of 1.8 MHz. Apoptosis cells were evaluated by light microscope and in situ terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling （TUNEL） and the expression level of p53 protein, bcl-2 protein, caspase-3, Fas protein and Fas L protein were tested by the flow cytometry （FCM） . Results Typical morphological changes of apoptosis such as apoptotic body were found under light microscope and the incidence of cell apoptosis and positive rates of p53 protein, caspase-3, Fas protein and Fas L protein in ceils exposure to 10 mV× 10 rain at 12h, 24h posttreatment were respectively higher than those in the ceils without treatment （P〈0. 001）, and positive rates of bcl-2 protein were lower than those in the no treatment ceils （P〈0. 001） Conclusions Ultrasound can induce K562 apoptosis in vitro, which may he related to increase of expression of p53 protein, caspase-3, Fas protein and Fas L protein and reduction of expression of bcl-2 protein.

关 键 词：凋亡 K562细胞 

分 类 号：R733.7[医药卫生—肿瘤]