CAJ | 학술논문

目的探讨肿瘤坏死因子相关凋亡诱导配体( TRAIL)对白血病NB4和K562细胞的作用及与其受体表达的关系.方法以Jurkat细胞株为阳性对照,采用不同浓度的TRAIL分别作用于NB4和K562细胞,观察细胞形态；采用四甲基偶氮唑蓝(MTT)比色法检测细胞生长情况；用流式细胞术检测细胞表面TRAIL受体的表达情况.结果 TRAIL作用导致NB4细胞株生存率显著下降,但弱于Jurkat细胞株,其变化具有TRAIL作用时间和浓度依赖性；对K562细胞株生存率的影响不明显.NB4细胞表面死亡受体4( DR4)和DR5表达水平较高,同时诱骗受体1(DcR1)表达较高；K562细胞DR5表达水平较高,而DR4及DcR1微量表达；Jurkat细胞表面仅DR5低水平表达；DcR2在三株细胞表面均无表达.结论 NB4细胞对TRAIL中度敏感,K562细胞对TRAIL耐受；NB4细胞敏感性较低可能与DcR1表达有关,K562细胞耐受性与其表面TRAIL受体表达无关.
목적 탐토종류배사인자상관조망유도배체( TRAIL)대백혈병NB4화K562세포적작용급여기수체표체적관계.방법 이Jurkat세포주위양성대조,채용불동농도적TRAIL분별작용우NB4화K562세포,관찰세포형태；채용사갑기우담서람(MTT)비색법검측세포생장정황；용류식세포술검측세포표면TRAIL수체적표체정황.결과 TRAIL작용도치NB4세포주생존솔현저하강,단약우Jurkat세포주,기변화구유TRAIL작용시간화농도의뢰성；대K562세포주생존솔적영향불명현.NB4세포표면사망수체4( DR4)화DR5표체수평교고,동시유편수체1(DcR1)표체교고；K562세포DR5표체수평교고,이DR4급DcR1미량표체；Jurkat세포표면부DR5저수평표체；DcR2재삼주세포표면균무표체.결론 NB4세포대TRAIL중도민감,K562세포대TRAIL내수；NB4세포민감성교저가능여DcR1표체유관,K562세포내수성여기표면TRAIL수체표체무관.
Objective To investigate the effect of TRAIL on NB4 and K562 cell lines, and its relationship with TRAIL releptors.Methods Jurkat cells were used as positive control,NB4 and K562 cells were treated with different concentrations of TRAIL. Cell morphologic changes were monitored. The cell proliferation was evaluated by MTT assay. The expression of TRAIL receptor were determined by flow cytometry.Results MTT assay showed that TRAIL inhibited the growth of NB4 and Jurkat cells in vitro in a dose-and time-dependent manner,but the effect of TRAIL on Jurkat cells was stronger than that on NB4 cells.However, the growth of K562 was not inhibited. Flow cytometry analysis revealed that DR4,DR5 and DcR1 were expressed higher in NB4 and K562 cells, but the levels of DR4 and DcR1 were very low in K562 cells.DR5 was expressed in Jurakat cells with low level. No DcR2 was detected on the surface of all the three cell lines.Conclusion NB4 cell line is moderately sensitive to TRAIL,and K562 cell line is resistant to TRAIL.The sensitivity of NB4 cells to TRAIL may be associated with the expression of DcR1, but the sensitivity of K562 cells have nothing to do with the expression of TRAIL receptors.