摘要
目的研究内质网应激对冬凌草甲素处理的肝癌细胞HepG2的作用。方法采用特异性小干扰RNA(siRNA)转染HepG2细胞72 h抑制内质网应激蛋白RNA激活蛋白激酶样内质网激酶(PERK)、抑制物阻抗性酯酶1(IRE-1)和CCAAT增强子结合蛋白同源蛋白(CHOP)表达后,MTT法观察40μmol·L-1冬凌草甲素处理12h的转染细胞的细胞存活率。结果 PERK和IRE-1 siRNA转染抑制相应蛋白表达后增加冬凌草甲素诱导的HepG2细胞死亡(P<0.05);而抑制CHOP表达对冬凌草甲素处理的HepG2细胞存活率没有影响(P>0.05)。结论冬凌草甲素诱导的内质网应激对HepG2细胞具有保护作用。
Objective To investigate the role of endoplasmic reticulum（ER） stress in oridonin-treated HepG2 cells. Methods We used small interfering RNA （siRNA） for the transfection of HepG2 cells for 72 h to knockdown the ex-pression of ER stress proteins such as RNA-activated protein kinase-like endoplasmic reticulum kinase（PERK）, in- hibitor resistant esterase 1 （IRE- 1 ） and CCAAT/enhancer-binding protein homologous protein （CHOP）. The cell via- bility of transfected HepG2 cells with 40 μmol ·L^-1 oridonin treatment for 12 h was evaluated by MTT assay. Results Knockdown of PERK or IRE-1 with specific siRNA increased oridonin- induced cell death （P 〈 0.05）, while sup pression of CHOP expression showed no effect on cell viability（P 〉 0.05）. Conclusion Oridonin-induced ER stress shows protective effect on HepG2 ceils.
出处
《中药新药与临床药理》
CAS
CSCD
北大核心
2012年第3期263-266,共4页
Traditional Chinese Drug Research and Clinical Pharmacology
基金
广东省2011年建设中医药强省科研课题(20111250)
