中文摘要：

目的研究20（S）-原人参二醇（aPPD）诱导人胶质瘤细胞U87凋亡的分子生物学机制。方法采用MTS法检测不同浓度aPPD对U87细胞的抑制作用，并用免疫印迹法研究caspase3的激活情况。结果不同浓度的aPPD对U87细胞均有杀伤或抑制作用，免疫印迹结果显示pro—caspase3在aPPD作用时减少，cas—pase3底物PARP发现被切割，说明caspase3被激活。结论aPPD能通过激活caspase3的方式诱导U87细胞凋亡。

英文摘要：

Objective： To investigate the molecular mechanism of aPPD induced apoptosis of U87. Methods： The cytotoxic effect of aPPD in gradient concentration were detected by the MTS assay. The activation of caspase3 in U87 was explored by means of immunoblotting. Results： aPPD can cause dose-dependent cytotoxicity to U87. The amount of pro-caspase3 decreased after aPPD treatment. In addition,cleaved band of PARP,a classic substrate, of caspase3,was demonstrated,indicating caspase3 was activated in U87. Conclusion： aPPD is capable of inducing apoptosis of U87 through activating caspase3.