青蒿酯钠诱导人肿瘤细胞凋亡及其分子机制的探讨  

Induction of human tumor cell apoptosis by sodium artesunate and its molecular mechanism

作　　者：杨小平[1] 张星[1] 

机构地区：[1]中山医科大学肿瘤研究所,广东广州510016

出　　处：《中草药》2002年第9期819-821,共3页Chinese Traditional and Herbal Drugs

基　　金：广东省自然科学基金资助项目 ( 970 0 87)

摘　　要：目的　研究青蒿酯钠诱导人肝癌细胞凋亡作用及探讨青蒿酯钠诱导人肝癌细胞凋亡的分子机制。方法　肝癌细胞 (BEL- 740 2 )经药物处理后 ,用荧光显微镜、透射电镜和流式细胞仪分析诱导凋亡作用 ,采用 Westernblot检测 p5 3、p2 1和 bc1- 2。结果　与对照组相比 ,经青蒿酯钠处理后 ,肝癌细胞中 p5 3、p2 1蛋白表达水平无明显变化 ,而 bc1- 2蛋白表达水平降低。结论　青蒿酯钠可诱导人肝癌细胞 (BEL- 740 2 )凋亡 ,其凋亡的分子机制是p5 3非依赖性的 ,即与 p5 3、p2 1无关 ,而与凋亡调节基因 bc1- 2下调有关。Object To study the apoptosis induced by sodium artesunate (SA) in human liver cancer cells and its molecular mechanism. Methods Induction of the apoptosis was analyzed by fluorescent microscope, transmission electron micrograph and flow lytometry based on drug treated BEL-7402. Expressions of p53, p21 and bc1-2 were determined by Western blot. Results The expression level of p53 and p21 had no change remarkbly, but the expression level of bc1-2 was reduced compared to that of the control group after the human liver cancer cells were treated by SA. Conclusion The apoptosis in human liver cancer cells (BEL-7402) may be induced by SA, the molecular mechanism of apoptosis may be p53-independent, that is no relative to p53 and p21. Otherwise, it is relative to bc1-2 down-regulation.

关 键 词：细胞凋亡 分子机制 肝癌 青蒿酯钠 肿瘤细胞 抗疟药物 实验研究 

分 类 号：R735.7[医药卫生—肿瘤] R978.61[医药卫生—临床医学]