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Hsp70.1在冬凌草甲素处理的肝癌细胞中的作用研究

Study of the role of Hsp70.1 in oridonin-treated hepatocarcinoma cells
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摘要 目的研究Hsp70.1在冬凌草甲素处理后的肝癌细胞HepG2中的表达情况及其与冬凌草甲素抗肿瘤活性的关系。方法采用蛋白印迹法及实时荧光定量PCR技术观察Hsp70.1在冬凌草甲素处理的肝癌细胞HepG2的表达变化,并采用RNA干扰技术观察抑制Hsp70.1表达后对冬凌草甲素抗肝癌效果的影响。结果冬凌草甲素作用12 h后,HepG2细胞的Hsp70.1蛋白及RNA表达均增加。Hsp70.1短发夹RNA(shRNA)转染抑制Hsp70.1表达后,与对照组相比,Hsp70.1 shRNA转染组、冬凌草甲素处理组或两者联合应用组的HepG2细胞的存活率均明显降低。结论 Hsp70.1可促进HepG2细胞的生存,对HepG2细胞和冬凌草甲素处理的HepG2细胞具有保护作用。 Objective To explore the expression of Hsp70.1 in oridonin-treated hepatocarcinoma HepG2 cells and the correlation of Hsp70.1 with the anticancer activity of oridonin.Methods By using Western blot and real-time PCR analysis,we tested the expression of Hsp70.1 protein and mRNA in HepG2 cells treated with oridonin.After HepG2 cells were transfected with Hsp70.1 shRNA,the influence of Hsp70.1 on the anticancer activity of oridonin was investigated.Results The levels of Hsp70.1 protein and mRNA increased in oridonin-treated HepG2 cells.Transient transfection of Hsp70.1-specific shRNA suppressed Hsp70.1 expression.Compared with control cells,Hsp70.1 shRNA-transfection,oridonin-treatment and combination of both-treatment groups significantly reduced cell viability.Conclusion Hsp70.1 upregulation contributes to HepG2 cells survival,which suggests that Hsp70.1 acts as a protective factor in both HepG2 cells and oridonin-treated HepG2 cells.
出处 《广东药学院学报》 CAS 2011年第4期423-426,共4页 Academic Journal of Guangdong College of Pharmacy
基金 香港浸会大学研究基金(FRG/08-09/I-08) 重大新药创制科技重大专项(2009ZX09103-708)
关键词 热休克蛋白70.1 冬凌草甲素 肝癌细胞 Hsp70.1 oridonin hepatocarcinoma cells
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