放线菌素D不能抑制α-双炔失碳酯诱导的白血病K562细胞凋亡  

α anordrin induced apoptosis of leukemia K562 cells is not prevented by actinomycin D

作　　者：楼丽广[1] 胥彬[1] 

机构地区：[1]中国科学院上海药物研究所

出　　处：《中国药理学通报》1997年第3期213-216,共4页Chinese Pharmacological Bulletin

基　　金：国家自然科学基金

摘　　要：目的：研究放线菌素Ｄ（ＡｃｔＤ）对α－双炔失碳酯（α－ａｎｏｒｄｒｉｎ，ＡＮＯ）诱导的人白血病Ｋ５６２细胞凋亡的影响。方法：用光学显微镜观察细胞形态学变化；用流式细胞仪、琼脂糖凝胶电泳分别检测ＤＮＡ含量和ＤＮＡ断裂。结果：ＡＮＯ５０μｍｏｌ·Ｌ－１处理人白血病Ｋ５６２细胞２４ｈ引起大约１０％Ｋ５６２细胞产生凋亡。同时加入ＲＮＡ合成抑制剂ＡｃｔＤ０．００５μｍｏｌ·Ｌ－１不能抑制ＡＮＯ诱导的凋亡，相反地，ＡｃｔＤ加强ＡＮＯ的这一作用，使凋亡细胞从１０％上升到２０％。ＡｃｔＤ０．５μｍｏｌ·Ｌ－１本身可诱导约３２％的Ｋ５６２细胞凋亡。Ｓ期细胞对ＡＮＯ诱导的凋亡较敏感，而ＡｃｔＤ则较易诱导Ｓ期和Ｇ２－Ｍ期细胞凋亡。结论：ＡＮＯ诱导的Ｋ５６２细胞凋亡不依赖于新的ＲＮＡ合成。AIM: To investigate the effect of actinomycin D (Act D) on the apoptosis induced by α anordrin (ANO) in human leukemia K562 cells. METHODS: Morphological changes were observed with light microscope; DNA content was measured by flow cytometry and DNA fragmentation analyzed by agarose gel electrophoresis. RESULTS: Exposure of K562 cells to ANO 50 μmol·L -1 for 24 h resulted in 10% cell apoptosis. RNA synthesis inhibitor, Act D 0 005 μmol·L -1 did not suppress ANO induced apoptosis. On the contrary, Act D augmented induction of apoptosis by ANO, causing an increase in apoptosis from 10% to 20%. Act D 0 5 μmol·L -1 itself induced 32% apoptosis of K562 cells. Cells in S phase were more sensitive to apoptosis in the presense of ANO, whereas Act D preferentially stimulated S and G 2 M Phase cells to undergo apoptosis. CONCLUSIONS: ANO induced apoptosis was not dependent on the synthesis of de novo RNA.

关 键 词：Α-双炔失碳酯 细胞凋亡 放线菌素D 白血病 

分 类 号：R733.7[医药卫生—肿瘤] R979.1[医药卫生—临床医学]