大黄素抑制食管癌EC-109细胞增殖的机制探讨

The Mechanism about the Inhibition Effects of Emodin on the Proliferation of EC-109 Cell in Esophageal Cancer

目的:探讨大黄素对人食管癌细胞株EC-109增殖和凋亡的影响,并初步探讨其作用机制。方法:不同浓度(0.0,2.5、5.0、10.0、20.0μg/mL)大黄素作用食管癌细胞EC-109,应用噻唑蓝比色法检测大黄素对食管癌细胞增殖的影响;用Annexin V-FITC/碘化丙啶双染流式细胞术检测细胞凋亡情况;流式细胞术检测细胞内活性氧变化情况。结果:不同浓度大黄素可明显抑制EC-109细胞增殖,并且呈浓度-时间依赖性;在作用EC-109细胞2 h后,细胞内活性氧明显增加;12 h后可见细胞凋亡率分别为8.1%、15.6%、24.0%、36.5%。结论:大黄素能明显抑制EC-109细胞的增殖,通过诱导细胞内活性氧的产生引起食管癌细胞EC-109凋亡。

Objective： To investigate the effects of emodin on esophageal cancer cell line EC-109 apoptosis, and to explore its mechanism. Methods： EC-109 cells were treated with different concentrations（0.0, 2.5, 5.0, 10.0, 20.0 μg/mL）of emodin. MTT assay was used to evaluate the influence of emodin on cell proliferation. Annexin V-FTTC and propidium iodide were used to stain EC-109 cells, and the flow cytometry was used to determine apoptosis after treatment of emodin. The flow cytometry was used to test intracellular reactive oxygen species levels. Results： Emodin obviously suppressed proliferation of EC-109 cells. The apoptosis ratio was 8.1%, 15.6%, 24.0% and 36.5% respectively when the concentration of emodin exposed was 2.5, 5.0, 10.0 and 20.0 μg/mL. The generation of reactive oxygen species in EC-109 ceils treated with emodin for 2 hours was enhanced significantly. Conclusion： Emodin can induce apeptosis in EC-109 cells, and the generation of reactive oxygen species is an important event involved in the apoptotic pathway induced by emodin.