摘要
菊科植物肿柄菊中富含tagitinin D,该化合物具有较强的抑制肿瘤细胞的作用。本文研究了tagitinin D诱导HepG2细胞凋亡的作用机制。采用克隆形成实验检测细胞成瘤能力、流式细胞仪测细胞周期及凋亡,DCFH-DA探针测活性氧的水平及Western blot检测ER stress相关蛋白表达。结果表明,tagitinin D抑制细胞成瘤,将细胞周期阻滞在G2/M期,诱导细胞凋亡,使细胞内ROS积累,增加了ER stress伴侣蛋白PDI、Calnexin、Ero1-Lα、Bip的表达并激活了IRE1α和PERK信号通路。综上所述tagitinin D依赖于ROS途径激活ER stress诱导细胞凋亡。
Tagitinin D was identified as one of the main compounds present in Asteraceae,which exhibited anti-tumor activities.To explore the mechanism of apoptosis in HepG2 cells induced by tagitinin D,colony formation assay was used to detect the cell proliferation ability.Then the cell cycle and apoptosis were checked by flow cytometry,and the changes of reactive oxygen species(ROS) levels was detected by DCFH-DA,and ER stress-related protein expression levels were determined using Western blot assay.The results showed that tagitinin D increased ROS levels,inhibited the cell proliferation,arrested the cell cycle in the G2/M phase,and induced apoptosis in HepG2 cells.ER stress signaling pathway related protein levels such as PDI,Calnexin,Ero1-Lα,Bip,IRE1-Lα,and p-eIF2α are increased.In summary,all the data suggested tagitinin D induced ROS which further elicited ER stress response and led to apoptosis in HepG2 cells.
作者
杨珊
韦睿然
陈远志
杨旭
王娟
杨杏芝
何志旭
丁骁
YANG Shan;WEI Rui-ran;CHEN Yuan-zhi;YANG Xu;WANG Juan;YANG Xing-zhi;HE Zhi-xu;DING Xiao(Department of Immunology,Basic Medical College,Tissue Engineering and Stem Cell Research Center,Guizhou Medical University,Guiyang 550004,China;State Key Laboratory of Phytochemistry and Plant Resources in West China,Kunming Institute of Botany,Chinese Academy of Sciences,Kunming 650201,China)
出处
《天然产物研究与开发》
CAS
CSCD
北大核心
2020年第3期359-364,共6页
Natural Product Research and Development
基金
国家自然科学基金(81703393)。
