中文摘要：

瞄准：学习新活跃 5 烷基树脂分的细胞毒性的机制[1， 3-dihydroxy-5-(tridec-4' ， 7'-dienyl ) 苯] 在肝肿瘤房间上从 Lithraea molleoides 叶子孤立。方法：在文化的人的 hepatocarcinoma 房间线(HepG2 和 Hep3B ) 与禁止的集中被对待， 50% 化合物，为 24 h。apoptosis 的正式就职被 DNA 破碎， DNA 内容，并且吖啶橙和 propidium 碘化物染色的分析在对待的房间检测。结果：在 5 烷基树脂分处理的 24 h 以后，两根房间线出现了：(1 ) apoptosis 的典型词法改变；(2 ) DNA 破碎，由流动血细胞计数由一张 subG0 人口的 laddering 和外观检测了；并且(3 ) 压缩了并且碎裂由氮蒽 orange-propidium 碘化物染色的原子核。结论：基于结果，这混合物通过 apoptotic 在两根肝细胞房间线施加它的细胞毒素的效果细胞死亡。为 Hep3B，有变异的 p53 和船边交货的房间， apoptosis 将由 p53 独立或船边交货无关的小径继续。

英文摘要：

AIM： To study the mechanism of cytotoxicity of a new active 5-alkyl resorcinol [1, 3-dihydroxy-5- （tridec-4＇, 7＇ -dienyl） benzene] isolated from Lithraea molleoides leaves on liver tumor cells. METHODS： Human hepatocarcinoma cell lines （HepG2 and Hep3B） in culture were treated with inhibitory concentrations, 50% of the compound, for 24 h. The induction of apoptosis was detected in treated cells by analysis of DNA fragmentation, DNA content, and acridine orange and propidium iodide staining. RESULTS： After 24 h of 5-alkyl resorcinol treatment, both cell lines showed： （1） the typical morphological alterations of apoptosis, （2） DNA fragmentation, detected by laddering and appearance of a subG0 population by flow cytometry, and （3） condensed and fragmented nuclei by acridine orange-propidium iodide staining. CONCLUSION： Based on the results, this compound exerts its cytotoxic effect in both hepatocellular cell lines through apoptotic cell death. For Hep3B, cells with mutated p53 and Fas, apoptosis would proceed by p53- or Fas-independent pathways.