环孢菌素A和Bcl-2高表达对EGTA诱导HL-60细胞凋亡的影响  

Effects of Cyclosporine A and Highly Expressed Bcl-2 on Apoptosis of HL-60 Cells Induced by EGTA

作　　者：马靖[1] 符乃阳[2] 徐安龙[1] 

机构地区：[1]中山大学生命科学学院生物化学系,广州510275 [2]广东省药品检验所,广州510180

出　　处：《生物化学与生物物理学报》2001年第2期251-255,共5页

基　　金：广州市科委重点项目!(No .97 Z 12 0 1);国家新药博士创新基金! (No .96 90 1 0 6 36 )资助&&

摘　　要：研究线粒体PT孔专一抑制剂环孢菌素A(CsA)和Bcl 2高表达对EGTA诱导HL 6 0细胞凋亡的影响。流式细胞仪检测凋亡峰、染色质凝聚的PI和Hoechst33342荧光双染观察、DNA梯状条带分析均表明 ,CsA明显促进EGTA诱导的HL 6 0细胞凋亡 ,而Bcl 2高表达完全阻断细胞凋亡的发生。借助荧光探针rhodamine 12 3和CMXRos研究细胞凋亡过程线粒体Δψm 的变化 ,结果表明HL 6 0细胞凋亡过程伴随线粒体Δψm 下降 ,CsA促进线粒体Δψm 下降 ,而Bcl 2高表达使HL 6 0细胞的线粒体Δψm 提高了近 1倍 。Effects of mitochondrial permeability transition pore specific inhibitor cyclosporine A (CsA) and highly expressed Bcl 2 on the apoptosis of HL 60 cells induced by EGTA were studied. Detection of apoptotic peak by flow cytometry, fluorescent microscope observation of chromatin condensation with double staining of PI and Hoechst33342 and DNA ladder analysis all demonstrated that CsA obviously enhanced the apoptosis of HL 60 cells induced by EGTA, while highly expressed Bcl 2 completely blocked it. It is revealed by mitochondrial membrane potential (Δψ m) fluorescent probes rhodamine 123 and CMXRos that the Δψ m decreased in the apoptosis of HL 60 cells induced by EGTA. CsA enhanced the decrease of Δψ m, but highly expressed Bcl 2 increased Δψ m of HL 60 cells about 2 fold and completely blocked the decrease of Δψ m.

关 键 词：细胞凋亡 线粒体PT孔 环孢菌素A BCL-2 HL-60 

分 类 号：Q25[生物学—细胞生物学]