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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(40,80,120μmol.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、AnnexinⅤ-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 observe the effect of emodin on the apoptosis of human colorectal cancer cell line LOVO and to explore whether reactive oxygen species (ROS) mediated the process of emodin-induced apoptosis. Methods Human colorectal cancer cell line LOVO was divided into three groups: blank control group and emodin group (40, 80, 120μmol.L-) 1, respectively. Emodin intervention time was 12, 24 and 48 h respectively. Cell proliferation rate was detected by MTT assay. Apoptosis was detected by Annexin Ⅴ-FITC and PI double staining flow cytometry. ROS level was detected by laser scanning confocal microscopy. Caspase-3 expression. Results Compared with the blank control group, the emodin intervention group induced apoptosis of LOVO cells in a concentration-dependent manner, the intracellular ROS level was significantly increased, and caspase-3 expression was significantly increased (P <0.05) . Conclusion Emodin induces apoptosis of colorectal cancer cells through ROS-mediated mitochondrial apoptosis signaling pathway, which may be one of the pathways of apoptosis induction in colorectal cancer cells.