Department of Applied Biology and Chemical Technology, The Hong Kong Polytechnic University, Hong Kong, China.
Inflammopharmacology. 2014 Apr;22(2):127-34. doi: 10.1007/s10787-013-0186-4. Epub 2013 Aug 22.
This study investigated the mechanism of the cytotoxic effect of emodin, an active anthraquinone, on human lung adenocarcinoma A549 cells. In vitro growth inhibition and suppression on colony forming were used to evaluate the effects of emodin on A549 cells. Emodin's ability in changing the expressions of apoptosis-related genes was studied by real-time RT-PCR. Emodin could significantly inhibit the growth of A549 cells with IC50 = 16.85 μg/ml (60 μM). It also concentration dependently inhibited the colony-forming ability of A549 cells with IC50 = 7.60 μg/ml (30 μM). Hallmarks of apoptosis, such as single-strand DNA breakage and DNA fragmentation, were observed in A549 cells treated with emodin. Emodin (72 h) treatment could up-regulate the gene expression of FASL (p < 0.05) and down-regulate the gene expression of C-MYC (p < 0.01), but induce no significant changes in the gene expressions of MCL1, GAPDH, BAX and CCND1. These results suggest that emodin could induce growth inhibition and apoptosis in A549 cells through modifying the extrinsic apoptotic pathways and the induction of cell cycle arrest.
本研究旨在探讨大黄素（一种有效的蒽醌类化合物）对人肺腺癌细胞 A549 的细胞毒性作用机制。通过体外生长抑制和集落形成抑制实验评估大黄素对 A549 细胞的作用。通过实时 RT-PCR 研究大黄素改变凋亡相关基因表达的能力。大黄素可显著抑制 A549 细胞的生长，IC50 = 16.85 μg/ml（60 μM）。它还浓度依赖性地抑制 A549 细胞的集落形成能力，IC50 = 7.60 μg/ml（30 μM）。在大黄素处理的 A549 细胞中观察到凋亡的特征性标志，如单链 DNA 断裂和 DNA 片段化。大黄素（72 h）处理可上调 Fasl 基因的表达（p < 0.05），下调 C-Myc 基因的表达（p < 0.01），但对 Mcl1、GAPDH、Bax 和 Ccnd1 基因的表达没有显著影响。这些结果表明，大黄素可能通过改变外源性凋亡途径和诱导细胞周期停滞来诱导 A549 细胞的生长抑制和凋亡。
