Chang Zhengqi, Xing Junchao, Yu Xiuchun
Tumour Biol. 2014 Jan;35(1):753-8. doi: 10.1007/s13277-013-1102-7.
The antitumor effects of curcumin have attracted widespread attention worldwide. One of its major functions is to induce the apoptosis of tumor cells, but the antitumor mechanism is currently unclear. In the present study, we found that cell mortality and curcumin concentration were dose dependent. Curcumin of low concentrations (10 μΜ) could reduce the level of reactive oxygen species (ROS) in tumor cells, while curcumin of high concentrations (80 μΜ) was able to significantly increase the content of ROS. In addition, Western blotting detection suggested that curcumin of high concentrations can induce the release of Cyto-C and the activation of Caspase-3, and that ROS scavenger NAC apparently inhibits apoptosis protein release and activation, consequently slowing the curcumin-induced apoptosis. Taken together, curcumin further activates the mitochondrial apoptotic pathway by inducing cells to generate ROS and ultimately promotes the apoptosis of tumor cells.
姜黄素的抗肿瘤作用已引起全球广泛关注。其主要功能之一是诱导肿瘤细胞凋亡,但其抗肿瘤机制目前尚不清楚。在本研究中,我们发现细胞死亡率与姜黄素浓度呈剂量依赖性。低浓度(10μΜ)的姜黄素可降低肿瘤细胞中的活性氧(ROS)水平,而高浓度(80μΜ)的姜黄素能够显著增加ROS的含量。此外,蛋白质免疫印迹检测表明,高浓度的姜黄素可诱导细胞色素C(Cyto-C)释放及半胱天冬酶-3(Caspase-3)激活,而ROS清除剂NAC明显抑制凋亡蛋白的释放和激活,从而减缓姜黄素诱导的细胞凋亡。综上所述,姜黄素通过诱导细胞产生ROS进一步激活线粒体凋亡途径,最终促进肿瘤细胞凋亡。