南京大学学报(自然科学版) ›› 2012, Vol. 48 ›› Issue (3): 360–366.
• • 上一篇
叶思思1，高静1**，龚爱华2，张严2，王穆彬2，杨小明3
Ye Si-Si1，Guo Jing1，Gong Ai一Hua2，Zhang Yan2,Wang Mu-Bing2,Yang Xiao-Ming3
摘要： 探讨银杏酸(Ginkgolic acids, GAs)诱导人肝癌细胞HepG2凋亡的效应，初步探索其与线粒体相互作用的机制.以不同浓度的GAs作用于HepG2 , MTT检测与相差显微镜观察相结合，分析GAs对细胞增殖的影响;Hochest染色观察细胞核变化;Annexin V /PI 双标后流式细胞仪检测凋亡情况; Western blot检测凋亡相关蛋白(Caspas-3 , Bax, Bcl-2)的表达;JG-1染色检测线粒体膜电位;DCFH-DA 染色检测活性氧(ROS)生成.结果发现，GAs、以时间和剂量依赖性方式抑制细胞的增殖;GAs处理诱导
HepG2细胞发生凋亡:细胞核皱缩及片段化，Caspase-3活化，Bax/Bcl-2比值增加，细胞凋亡率显著上升.此外，GAs可直接与线粒体发生作用，诱导HepG2细胞线粒体外膜膜电位下降，PTP孔道开放，ROS含量升高.研究结果表明GAs能够诱导肝癌细胞的凋亡，推测其主要通过影响线粒体功能而导致细胞的凋亡.
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