论文部分内容阅读
探讨微波和足叶乙甙体外诱导K562细胞凋亡的可能性及其机制。方法 :将微波和足叶乙甙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及p21ras蛋白阳性率的测定来评价细胞凋亡的程度并研究其机制。结果 :微波和足叶乙甙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甙有显著性增加 (P<0 05),其中K562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及 p21ras蛋白阳性率的降低是同步的。结论 :微波和足叶乙甙共同作用于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蛋白及p21ras蛋白阳性率的降低有关
To explore the possibility and mechanism of microwave and etoposide inducing K562 cell apoptosis in vitro. Methods: Microwave and etoposide were used alone and in combination with normal bone marrow cells and K562 cells respectively. The degree of apoptosis and the mechanism of apoptosis were evaluated by measuring the apoptosis rate and the positive rate of bcl-2 and p21ras protein. Results: Microwave and etoposide each induced a small amount of apoptosis in normal myeloid cells and K562 cells, and the apoptosis rate induced by the combination of them was significantly higher than that of etoposide (P <0.05 ). The rate of apoptosis of K562 cells was much higher than that of normal bone marrow cells. The increase of apoptosis rate and the decrease of positive rates of bcl2 and p21ras proteins were synchronous. Conclusion: The combination of microwave and etoposide can induce a certain degree of synergistic effect in K562 cells. The induction of apoptosis is related to the decrease of the positive rate of bcl-2 protein and p21ras protein