CAJ | 학술논문

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.
목적:연구고과단백(momordin)유도인만성립세포백혈병내약세포주K562/A02적조망급작용궤제.방법:채용CCK-8법검측세포생장억제솔,FCM법화세포형태학검측세포조망,FCM법검측P-당단백(P-glycoprotein, P-gp)、p53、bcl-2화caspase-3단백표체수평,병운용caspase-8활성검측시제합검측caspase-8적활성.결과:고과단백능억제K562/A02내약세포적생장차정제량의뢰관계,병능유도세포조망,능사P-gp、p53화bcl-2적표체하강,이사caspase-3화caspase-8활성증강.결론:고과단백가역전내약세포주K562/A02적세포조망수억성,주요궤제가능여기하조p53、P-gp화bcl-2적표체이급제고caspase활성유관.
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.