【摘要】 目的:研究苦瓜蛋白(momordin)诱导人慢性粒细胞白血病耐药细胞株K562/A02的凋亡及作用机制。方法:采用CCK-8法检测细胞生长抑制率,FCM法和细胞形态学检测细胞凋亡,FCM法检测P-糖蛋白(P-glycoprotein,P-gp)、p53、bcl-2和caspase-3蛋白表达水平,并运用caspase-8活性检测试剂盒检测caspase-8的活性。结果:苦瓜蛋白能抑制K562/A02耐药细胞的生长且呈剂量依赖关系,并能诱导细胞凋亡,能使P-gp、p53和bcl-2的表达下降,而使caspase-3和caspase-8活性增强。结论:苦瓜蛋白可逆转耐药细胞株K562/A02的细胞凋亡受抑性,主要机制可能与其下调p53、P-gp和bcl-2的表达以及提高caspase活性有关。更多还原

【Abstract】 Objective:To study the molecular mechanism for momordin in inducing apoptosis of multidrug-resistant human chronic leukemia K562/A02 cells.Methods:The growth inhibition value of K562/A02 cells was detected by CCK-8 method.Cell apoptosis was analyzed by Annexin Ⅴ flow cytometry(FCM) and cell morphological examination.FCM was also used in determining expression of P-glycoprotein,p53 protein,bcl-2 protein and caspase activity.Results:Momordin inhibited the proliferation of K562/A02 cells in a dose-dependent manner.It also induced cell apoptosis,reduced the expression of P-glycoprotein,p53 protein and bcl-2 protein,and increased caspase-3 and caspase-8 activity.Conclusion:Momordin reversed the inhibition of apoptosis in multidrug-resistant K562/A02 cells.The molecular mechanism may be related with down-regulation of expression of p53 protein,P-glycoprotein,and bcl-2 protein and up-regulation of caspase-3 and caspase-8 activities.更多还原