目的 观察大黄素对人大肠癌细胞株LOVO凋亡的影响，并探讨活性氧(ROS)是否介导了大黄素诱导细胞凋亡的过程。方法 体外分组培养人大肠癌细胞株LOVO，设空白对照组和大黄素3个不同浓度干预组(40，80，120 μmol·L-1)，大黄素干预时间分别为12，24，48 h。以四甲基偶氮唑盐(MTT)法检测细胞增殖率、Annexin Ⅴ-FITC和PI双染流式细胞术检测凋亡，激光扫描共聚焦显微镜检测细胞内ROS水平，Western印迹法检测caspase-3表达。结果 与空白对照组比较，大黄素干预组呈浓度依赖性诱导大肠癌细胞株LOVO凋亡，细胞内ROS水平明显增加，caspase-3的表达明显上调，差异均有统计学意义(P ＜ 0.05)。结论 大黄素通过ROS介导线粒体凋亡信号通路诱导大肠癌细胞凋亡，可能是大肠癌细胞凋亡诱导途径之一。

Objective To investigate the influence of emodin on the apoptosis of human colon cancer cell line LOVO and to explore the role of reactive oxygen species(ROS) in this process. Methods The LoVo cells were divided into blank control group and emodin treatment groups(emodin at the concentrations of 40，80，120 μmol·L-1)，and the intervention time was 12，24，48 h，respectively. The proliferation of LOVO cells was assayed by methyl thiazolyl tetrazolium(MTT) method，and the apoptosis was detected by Annexin Ⅴ-FITC and PI double-staining flow cytometry. Cellular ROS level was detected by using a confocal laser scanning microscope. In addition，caspase-3 expression was analyzed by Western blotting method. Results Compared with the blank control group，emodin treatment groups induced the apoptosis(P＜0.05)，increased the level of ROS(P＜0.05) in human colon cancer cell line LOVO，and up-regulated the expression of caspase-3(P＜0.05)in dose-dependent manner，the difference being statistically significant(P＜0.05). Conclusion Emodin induces the apoptosis of human colon cancer cell line LOVO through ROS- mediated mitochondrial signaling pathway，which may be one of its apoptosis-inducing mechanisms.

R285.5