摘要
目的:研究维生素K2(VK2)对慢性粒细胞白血病急性变细胞株K562细胞的生长抑制作用及其机制。方法:采用形态学检测VK2作用后的细胞形态改变,MTT方法检测VK2对K562细胞的生长抑制作用,流式细胞仪Annexin-VFITC/PI分析细胞凋亡,PI染色分析细胞周期变化,RT-PCR技术检测抗凋亡基因bcl-2、促凋亡基因bax的表达。结果:经VK2作用后细胞出现明显的形态学改变:细胞变小,核固缩,核染色质聚集边挤于核膜内侧呈新月形以及典型凋亡小体形成等;MTT结果显示VK2对K562细胞有明显的抑制作用,作用72 h半数抑制浓度为25.1μmol.L-1;流式细胞仪检测结果显示随着VK2浓度的增加凋亡率逐渐增高(P<0.05),随着作用时间的延长凋亡率也逐渐增高(P<0.05);VK2作用72 h,S期细胞逐渐减少(r=-0.99,P<0.05),G0/G1期细胞逐渐增加(r=1.00),细胞被阻滞在G0/G1期;随着VK2浓度的增高抗凋亡基因bcl-2表达明显下调,而促凋亡基因bax表达无明显差异。结论:VK2通过诱导K562细胞凋亡抑制其增殖,并呈浓度和时间依赖性;抗凋亡基因bcl-2下调可能是VK2诱导K562细胞发生凋亡的机制之一。
Objective To study the inhibiting effects of vitamin K2 （ VK2 ） on the treatment of K562 cells and its possible mechanism. Methods The changes of morphologic features of K562 cells were observed. Cell apoptosis and cell cycle shift were also investigated by flow cytometry（FCM）. The expressions of apoptosis-related genes bcl-2 and bax were delected by retrotrans criptase polymerase chain reaction（RT-PCR）. Results Apoptosis peak on FCM and positive Aimexin-VFITC on cell membrane showed that VK2 induced apoptosis of K562 cell in a dose-and time-dependent manner, resulting in G0/G1 cell arrest; VK2 significantly down-regulated the apoptosis-related genes bcl-2 expression, but there were no changes of bax expression. Conclusion VK2 induces apoptosis of K562 cells and the apoptosis-related genes bcl-2 down-regulation might play an important role in this process.
出处
《东南大学学报（医学版）》
CAS
2005年第5期310-314,共5页
Journal of Southeast University(Medical Science Edition)
