摘要
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.
出处
《汕头大学医学院学报》
2009年第1期12-14,F0002,共4页
Journal of Shantou University Medical College
关键词
大黄素
食管癌
活性氧
凋亡
emodin, esophageal cancer, reactive oxygen specie, apoptosis