论文部分内容阅读
目的探讨大黄素联合顺铂诱导人食管癌EC-9706细胞凋亡过程中的作用及可能机制。方法不同浓度大黄素、顺铂与二药联合分别作用于EC-9706细胞,应用吖啶橙/溴化乙锭(AO/EB)双荧光染色法测细胞凋亡(形态学变化);MTT法检测细胞抑制率;用Annexin V-FITC/碘化丙啶(PI)双染法及流式细胞术检测细胞凋亡情况(计算凋亡细胞百分率);流式细胞术检测细胞内活性氧变化情况。结果大黄素、顺铂均可明显抑制EC-9706细胞增殖,并且呈一定的时间依赖性;大黄素、顺铂分别及联合作用24 h,细胞早期凋亡率分别为(15.39±3.40)%、(12.80±2.41)%和(23.09±3.97)%,较对照组〔(1.42±0.14)%〕明显增加(P均<0.05);两药分别及联合作用2 h,细胞内活性氧的含量分别为(35.57±3.16)%、(29.44±2.43)%和(43.23±3.68)%,较对照组〔(4.73±2.12)%〕明显升高(P<0.05)。结论大黄素能抑制EC-9706细胞增殖,通过诱导细胞内活性氧的产生促进凋亡,与顺铂联用存在协同作用,其机制可能与通过诱导细胞内活性氧的产生促进细胞凋亡有关。
Objective To investigate the role of emodin and cisplatin in inducing apoptosis of human esophageal carcinoma cell line EC-9706 and its possible mechanism. Methods EC-9706 cells were treated with different concentrations of emodin, cisplatin and two drugs respectively. Apoptosis (morphological changes) were detected by acridine orange / ethidium bromide staining (AO / EB) The cell apoptosis rate was detected by Annexin V-FITC / propidium iodide (PI) staining and flow cytometry (the percentage of apoptotic cells was calculated). The changes of intracellular reactive oxygen species (ROS) were detected by flow cytometry . Results Emodin and cisplatin could significantly inhibit the proliferation of EC-9706 cells in a time-dependent manner. The apoptosis rates of EC-9706 cells treated with emodin and cisplatin for 24 h were (15.39 ± 3.40)%, (12.80 ± 2.41)% and (23.09 ± 3.97)% respectively, which was significantly higher than that of the control group (1.42 ± 0.14%) (P all <0.05). The contents of intracellular reactive oxygen species (35.57 ± 3.16)%, (29.44 ± 2.43)% and (43.23 ± 3.68)% respectively, which was significantly higher than that in the control group (4.73 ± 2.12%) (P <0.05). Conclusion Emodin can inhibit the proliferation of EC-9706 cells and induce apoptosis through the induction of intracellular reactive oxygen species (ROS), which may be related to the synergistic effect of cisplatin and cisplatin. It may be related with the induction of intracellular reactive oxygen species (ROS).