^(131)I-GM-CSF诱导HL-60/ADM细胞凋亡机制研究

The mechanism of ^(131)I-GM-CSF inducing apoptosis of HL-60/ADM cells

目的:研究131I-GM-CSF诱导HL-60/ADM细胞凋亡机制。方法:采用体外放射免疫治疗模型,通过透射电子显微镜、流式细胞术及免疫细胞化学检测等方法,研究131I-GM-CSF辐射一定时间后HL-60/ADM细胞的凋亡率、凋亡形态学上的改变、相关基因的表达和线粒体膜电位的改变。结果:显示131I-GM-CSF可诱导HL-60/ADM细胞凋亡,在诱导细胞凋亡过程中,HL-60/ADM细胞超微结构明显破坏,细胞线粒体膜电位降低,Bax表达上调,Bcl-2、Bcl-xl表达下调。结论:131I-GM-CSF作为放射导向治疗药物能诱导HL-60/ADM细胞凋亡,具有抗白血病的作用,其诱导凋亡的机制与开放线粒体膜的通透性转换孔(MPT)、降低线粒体膜电位(MTP),上调Bax,下调Bcl-2、Bcl-xl有关。

Ohjective：To investigate the mechanism of ^131I-GM-CSF inducing apoptosis of HL-60/ADM cells. Methods：An in vitro radioimmunotherapy （RAIT） model was employed. Data were collected from transmission electrion microscopy, flow cytometric analysis and immnocytochemistry assay.Results：After exposure to ^131I-GM-CSF,HL-60/ADM cells were induced to apoptosis,The cell mitochondrial transmembrane potential（MTP）reduced and HL-60/ADM cells appeared the classical apoptotic morphology,The Bax was up regulated.while Bcl-2 and Bcl-xl was decreased.Conclusion;^131I-GM-CSF can induce HL-60/ADM apoptosis through opening the mitochondrial permeability transition pore and reducing MTP,which suggests that ^131I-GM-CSF may be available in therapy of AML.