微波和足叶乙苷体外诱导K562细胞凋亡的研究

STUDIES ON THE COMBINATION OF MICROWAVE AND ETOPOSIDE FOR INDUCING K562 CELL APOPTOSIS IN VITRO

探讨微波和足叶乙苷体外诱导Ｋ５６２ 细胞凋亡的可能性及其机制． 将微波和足叶乙苷分别单独以及联合作用于正常骨髓细胞和Ｋ５６２ 细胞株， 通过细胞凋亡率和ｂｃｌ２ 蛋白阳性率的测定来评价细胞凋亡的程度并研究其机制． 微波和足叶乙苷各自都能诱导正常骨髓细胞和Ｋ５６２ 细胞的少量凋亡， 两者联合作用所诱导的细胞凋亡率较之于足叶乙苷有显著性增加（Ｐ＜ ０ ．０５） ， 其中Ｋ５６２ 的细胞凋亡率的增加幅度远大于正常骨髓细胞； 细胞凋亡率的增加和ｂｃｌ－ ２ 蛋白阳性率的降低是同步的． 微波和足叶乙苷共同作用于Ｋ５６２ 细胞来诱导凋亡能够产生一定程度的协同效应， 这种凋亡的诱导作用与ｂｃｌ－ ２

To study the possibility and the mechanism of K562 apoptosis induced by microwave and etoposide. Methods: Normal human bone marrow cell and K562 cell line were treated by microwave and etoposide alone or by the combination of both. The ratio of apoptotic cell(RAC) and the ratio of bcl_2 protein positive cell(Rbcl_2PC) were measured in order to evaluate cell apoptosis and to study its mechanism. Results: Both microwave and etoposide could induce a little apoptosis of these two kinds of cells,while the combination of microwave and etoposide could induce a remarkable higher RAC than etoposide could do. ( P <0.05)At the same time, RAC for K562 increased much more higher than that for normal human bone marrow cell. RAC increased simultaneously with Rbcl-2PC reduction. Conclusion: The combination of microwave and etoposide showed a limited synergistic effect on inducing K562 apoptosis, and this effect was related to Rbcl-2PC reduction.