Bártová E, Spanová A, Janáková L, Bobková M, Rittich B
Institute of Pathological Physiology, Medical Faculty, Masaryk University, Brno, Czech Republic.
Physiol Res. 1997;46(2):155-60.
Apoptosis was induced by treatment of HL-60 cells with C2-ceramide. Apoptotic damage of DNA was detected according to the sub-G1 peak on a flow cytometer, according to the typical morphology and according to the DNA fragmentation "ladder" after gel electrophoresis. It was shown that the apoptotic cleavage followed after G1 blockade of the cell cycle. A high correlation coefficient (rs=0.957) was found between the percentages of G1 blocked cells and apoptotic cells. This high correlation together with the appearance of the sub-G1 peak suggests that the G1 blocked HL-60 cells were subject to apoptotic death. It is deduced that the mechanisms leading to G1 blockade of the cell cycle and activation of apoptosis in HL-60 cells are interconnected.
用C2-神经酰胺处理HL-60细胞可诱导细胞凋亡。根据流式细胞仪上的亚G1峰、典型形态以及凝胶电泳后的DNA片段化“梯形条带”检测DNA的凋亡损伤。结果表明，细胞凋亡裂解发生在细胞周期的G1期阻滞之后。在G1期阻滞细胞百分比与凋亡细胞百分比之间发现了较高的相关系数（rs = 0.957）。这种高度相关性以及亚G1峰的出现表明，G1期阻滞的HL-60细胞会发生凋亡死亡。由此推断，导致HL-60细胞周期G1期阻滞和凋亡激活的机制是相互关联的。
