氧化应激在姜黄素诱导肺癌细胞凋亡中的作用及机制研究  

Role and mechanism of oxidative stress on curcumin induces apoptosis in A549 cells

作　　者：姚庆华[1] 林妙[2] 汪玉琪[2] 来岳标[2] 陈寒露[2] 傅婷[2] 汪潞[2] 毛伟敏[1] 

机构地区：[1]浙江省肿瘤医院,杭州310022 [2]浙江中医药大学第一临床医学院,杭州310053

出　　处：《中华中医药杂志》2016年第2期614-618,共5页China Journal of Traditional Chinese Medicine and Pharmacy

摘　　要：目的:探讨姜黄素诱导肺癌A549细胞凋亡及其相关的氧化应激机制。方法:将不同浓度(5-40μmol/L)的姜黄素作用于肺癌细胞株A549细胞,以MTT法检测姜黄素不同浓度(5-40μmol/L)在不同时间点(3、6、12、24、48h)对A549细胞的抑制增殖率,流式细胞术检测细胞凋亡率;DCFH-DA探针染色流式检测细胞内活性氧(ROS)的变化,WST-1法检测细胞内超氧化物歧化酶(SOD),硫代巴比妥酸法检测丙二醛(MDA),ELISA法检测4-羟基壬烯酸(4-HNE)。结果:MTT法检测发现姜黄素对肺癌A549细胞的生长抑制作用呈剂量和时间依赖性,抑制率随姜黄素的浓度增高和处理时间延长而增加,应用PI及Annexin V-FITC双标记染色测定细胞凋亡发现凋亡率和坏死率也随着姜黄素的浓度增高而增加。姜黄素处理后胞内ROS显著降低,SOD活性显著升高,MDA、4-HNE活性显著下降,HSP70活性显著下降,Bax/Bcl-2比值显著增高。结论:姜黄素通过调节肺癌细胞内氧化还原状态来参与促进肿瘤细胞凋亡的机制。Objective：To explore the effects and molecular mechanism of curcumin inhibit growth and apoptosis in A549 human lung cancer cells.Methods：The cell viability was determined by MTT assay.The apoptosis and mitochondrial menberane potential were detected by flow cytometry.ROS was determined with DCFH-DA by flow cytometry,and SOD,MDA,4-HNE was separately detected by WST-1 method,malondialdehyde barbituric acid method and ELISA method.Results：Above 20umol/L concentrations of curcumin significantly inhibit the vitality in A549 cells for 24 h,induced the cell apoptosis,decreased obviously mitochondrial membrane potential,released cytochrome C into the cytoplasm,decline HSP70 activity,enhanced Bax/Bcl-2 ratio.Intracellular ROS significantly reduced,SOD activity increased and MDA,4-HNE activity decline.Conclusion：curcumin by adjusting the lung cancer cells within the REDOX state to participate in promoting mechanism of tumor cell apoptosis.

关 键 词：姜黄素 肺癌 凋亡 氧化应激 热休克蛋白70 

分 类 号：R285[医药卫生—中药学]