Department of Respiratory Disease, First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, PR China.
Oncol Rep. 2010 Feb;23(2):397-403.
Several studies have shown that curcumin can induce apoptosis and inhibit growth in human A549 lung adenocarcinoma cells. However, the mechanism is not completely understood yet. The present study was designed to investigate the effects of curcumin on A549 cells to better understand its apoptosis and apoptosis-related factors in vitro. The apoptosis induction, intracellular reactive oxygen species (ROS) and mitochondrial membrane potential (MMP) were examined by confocal fluorescence microscope and flow cytometry. The MAPK protein expression was examined by Western blot analysis. After treatment with curcumin, apoptosis were observed. Curcumin-induced apoptosis was accompanied by an increase of intracellular ROS level and a loss of MMP. In addition, induction of apoptosis was also accompanied by sustained phosphorylation and activation of JNK, p38 and ERK. However, pretreatment with MAPK inhibitors had no effect upon curcumin-induced apoptosis. GSH and NAC, an anti-oxidant agent, blocked the curcumin-induced ROS production, MMP loss and rescued cells from curcumin-induced apoptosis. Our results indicated that curcumin induced apoptosis in A549 cells through a reactive oxygen species-dependent mitochondrial signaling pathway and independent of MAPK signaling pathway.
多项研究表明姜黄素能诱导人 A549 肺腺癌细胞凋亡并抑制其生长。但作用机制尚未完全阐明。本研究旨在通过体外实验探讨姜黄素对 A549 细胞的作用,以更好地了解其凋亡及其相关因素。通过共聚焦荧光显微镜和流式细胞术检测细胞凋亡、细胞内活性氧(ROS)和线粒体膜电位(MMP)。通过 Western blot 分析检测 MAPK 蛋白表达。姜黄素处理后观察到细胞凋亡。姜黄素诱导的凋亡伴随着细胞内 ROS 水平的增加和 MMP 的丧失。此外,凋亡的诱导还伴随着 JNK、p38 和 ERK 的持续磷酸化和激活。然而,用 MAPK 抑制剂预处理对姜黄素诱导的细胞凋亡没有影响。GSH 和 NAC,一种抗氧化剂,阻断了姜黄素诱导的 ROS 产生、MMP 丧失,并使细胞免于姜黄素诱导的凋亡。我们的结果表明,姜黄素通过依赖于活性氧的线粒体信号通路诱导 A549 细胞凋亡,而不依赖于 MAPK 信号通路。