Department of Biological Science and Biotechnology, Tsinghua University, Beijing 100084, PR China.
Environ Toxicol Pharmacol. 2009 Jul;28(1):97-103. doi: 10.1016/j.etap.2009.03.005. Epub 2009 Mar 17.
We investigated possible mechanism(s) where honokiol induces apoptosis in human hepatocellular carcinoma SMMC-7721 cells. MTT assay showed that honokiol has strong inhibition on SMMC-7721 cells in a dose-dependent manner. SMMC-7721 cells after honokiol treatment display morphological characteristics such as cell shrinkage, detachment from the culture plate, formation of apoptotic bodies, change to a round shape, and marked nuclear condensation and fragmentation after 32258 staining. Cell apoptosis was measured by Annexin-V/PI staining and alternatively, by the subG0/G1 percentage of the cell cycle analysis followed by FACS. An obvious loss of ΔΨ(m) and a quick burst of ROS was detected when honokiol reached 4μg/ml, which was coincident with the high apoptosis percentage in our previous research. Up-regulation of Bax and down-regulation of Bcl-2 were observed, suggesting that honokiol-induced apoptosis was associated with reactive oxygen species (ROS) production and an increase of Bax/Bcl-2 ratios.
我们研究了厚朴酚诱导人肝癌 SMMC-7721 细胞凋亡的可能机制。MTT 法显示，厚朴酚对 SMMC-7721 细胞具有很强的抑制作用，呈剂量依赖性。经厚朴酚处理后的 SMMC-7721 细胞在吖啶橙染色后呈现出细胞收缩、从培养板上脱落、形成凋亡小体、变圆以及明显的核浓缩和碎裂等形态特征。通过 Annexin-V/PI 染色或细胞周期分析中的亚 G0/G1 百分比来测量细胞凋亡。当厚朴酚达到 4μg/ml 时，明显观察到 ΔΨ(m) 的丧失和 ROS 的快速爆发，这与我们之前研究中的高凋亡百分比相一致。观察到 Bax 的上调和 Bcl-2 的下调，提示厚朴酚诱导的凋亡与活性氧（ROS）的产生和 Bax/Bcl-2 比值的增加有关。
