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目的:探讨活性氧(reactive oxygen species,ROS)在蓝萼甲素(glaucocalyxin A,GLA)诱导的人慢性粒细胞白血病K562细胞毒性中的作用。方法:GLA(0.313,0.625,1.250,2.500,5.000,10.000 mg.L-1)处理K562细胞12,24,48 h后,噻唑蓝(MTT)法观察细胞毒作用;流式细胞术检测GLA(2.5,5.0,10.0 mg.L-1)对K562细胞周期的阻滞作用;流式细胞术检测5.0 mg.L-1 GLA作用后K562中的ROS变化;利用MTT法检测抗氧化剂氮乙酰半胱氨酸(N-acetylcysteine,NAC)对GLA诱导下K562细胞毒作用的影响;流式细胞术检测NAC对GLA诱导下K562细胞周期的影响。结果:GLA对K562细胞的生长抑制呈明显的剂量和时间依赖关系,12,24,48 h的IC50分别为6.168,2.968,1.086 mg.L-1;GLA对K562细胞周期的阻滞作用主要发生在G0/G1期;5.0 mg.L-1 GLA作用K562细胞2 h后ROS较空白组上升1.3倍;NAC对GLA细胞毒作用有明显的抑制作用,且随NAC浓度上升,抑制作用增强;NAC能减弱GLA对K562的细胞周期阻滞作用。结论:GLA对K562细胞具有细胞毒及细胞周期阻滞作用,且这些作用与ROS有关。
Objective: To investigate the role of reactive oxygen species (ROS) in glaucocalyxin A (GLA) -induced cytotoxicity of human chronic myeloid leukemia K562 cells. Methods: K562 cells were treated with GLA (0.313,0.625,1.250,2.500,5.000,10.000 mg.L-1) for 12, 24 and 48 hours, and the cytotoxicity was observed by MTT assay. 2.5, 5.0, 10.0 mg.L-1) on the cell cycle of K562 cells. The changes of ROS in K562 cells treated with 5.0 mg.L-1 GLA were detected by flow cytometry. The antioxidant acetylcysteine (NAC) on GLA-induced K562 cytotoxicity. The effect of NAC on GLA-induced K562 cell cycle was detected by flow cytometry. Results: GLA inhibited the growth of K562 cells in a time-and dose-dependent manner. The IC50 values of GLA at 12, 24 and 48 h were 6.168, 2.968 and 1.086 mg.L-1, respectively. GLA inhibited the cell cycle arrest of K562 cells mainly In G0 / G1 phase, the ROS of K562 cells increased by 1.3-fold after treated with 5.0 mg · L-1 GLA for 2 h. NAC inhibited the cytotoxicity of GLA significantly and increased with the increase of NAC concentration. NAC Can weaken GLA on K562 cell cycle arrest. Conclusion: GLA has cytotoxicity and cell cycle arrest on K562 cells, and these effects are related to ROS.