摘要
目的探讨牛蒡子苷元对小鼠红白血病细胞株FBL-3细胞凋亡的影响及机制。方法以小鼠红白血病FBL-3细胞为研究对象,以不加药的FBL-3细胞为对照组,20mg/L牛蒡子苷元处理24h的FBL-3细胞为实验组。通过琼脂糖凝胶电泳和流式细胞术观察牛蒡子苷元对小鼠红白血病FBL一3细胞凋亡的影响,通过反转录-聚合酶链反应(RT-PCR)法检测牛蒡子苷元处理前后FBL-3细胞凋亡相关基因表达的变化。结果电泳结果显示,与对照组相比,实验组可见明显的DNA“梯子”样断裂变化。流式细胞仪结果显示,与对照组相比,实验组细胞凋亡数量明显增加(t=60.681,P=0.000)。RT—PCR结果显示,与对照组相比,实验组细胞抗凋亡基因Bcl-2和lAP-J表达显著下调(t=14.732、29.702,P均=0.000),而Bcl—XL表达没有明显变化(t=0.209,P=0.844);促凋亡基因Box和Smac表达明显上调(t=6.721、8.499,P=0.003、0.001)。结论牛蒡子苷元可诱导FBL-3细胞凋亡,其机制可能与抗凋亡基因Bcl-2租IAP-J表达下调及促凋亡基因bax和Smac表达上调有关。
Objective To investigate the effect of arctigenin on the apoptosis of FBL-3 cells and its mecha- nisms. Methods The mouse erythroleukemia FBL-3 cells were taken as subjects. The untreated FBL-3 parental cells were taken as the control group, and the FBL-3 cells treated with 20 mg/L arctigenin for 24 h were taken as the experi- mental group. The effects of arctigenin on the apoptosis of the mouse erythroleukemia FBL-3 cells were determined by agarose gel electrophoresis and flow cytometry assay. The changes of apoptosis-related genes were analyzed by reverse transcriptase-polymerase chain reaction(RT-PCR). Results The agarose gel electrophoresis results revealed that the " DNA ladder" was displayed in the experimental group compared to the control group. The flow cytometry data demon- strated that the apoptosis number of FBL-3 cells in the experimental group was markedly increased compared to that in the control group (t = 60. 681, P = 0. 000). The RT-PCR assay results suggested that the expressions of Bcl-2 and IAP-1 gene were down-regulated in the experimental group compared to the control group (t = 14. 732,29. 702, all P = 0. 000), while the expressions of Bax and Smac gene were up-regulated( t = 6. 721,8. 499 ;P = 0. 003,0. 001 ) , but the expression of Bcl-XL did not change ( t = 0. 209, P = 0. 844 ). Conclusions Aretigenin can induce the apoptosis of the mouse erythrolenkemia FBL-3 cells. Apoptosis of the mouse erythrolenkemia FBL-3 cells induced by arctigenin may be correlated to the down-regulation of Bcl-2 and IAP-1 and up-regulation of Bax as well as Smac.
出处
《中华实用儿科临床杂志》
CAS
CSCD
北大核心
2013年第24期1895-1897,共3页
Chinese Journal of Applied Clinical Pediatrics