牡荆葡基黄酮调节TAK1/AMPK通路增强人肝癌细胞的放射敏感性  

Vitexin glucolone enhances radiosensitivity of hepatocellular carcinoma cell via TAK1/AMPK signaling pathway

作　　者：苏书娟 SU Shu-Juan(The First Affiliated Hospital of Nanyang Medical College,Nanyang 473000,Chin)

机构地区：[1]南阳医专一附院,南阳473000

出　　处：《中国免疫学杂志》2018年第8期1158-1162,共5页Chinese Journal of Immunology

基　　金：河南省科技攻关基金资助项目(971200100)

摘　　要：目的:探究牡荆葡基黄酮(VG)对人肝癌细胞放疗敏感性的作用及作用机制。方法:用不同浓度VG和放疗处理细胞,CCK8检测细胞活性,流式检测细胞凋亡,Western blot检测凋亡标记蛋白和TAK1/AMPK通路蛋白表达。TAK1 siRNA(si-TAK1)转染细胞,Western blot检测TAK1的表达,CCK8检测细胞活性,流式检测细胞凋亡。结果:VG和放疗均能明显抑制Huh7细胞的活性,且VG浓度为20μmol/L和40μmol/L时,其抑制作用优于放疗。VG可显著增强放疗对肝癌细胞凋亡的促进作用,并升高Bax/Bcl-2的比值。同时,VG还能增强放疗对TAK1/AMPK通路蛋白(TAK1、AMPKα1和PPARγ)表达的促进作用,下调TAK1表达能明显反转VG增强放疗促细胞凋亡活性及抑制细胞增殖活性的作用。结论:VG可通过TAK1/AMPK通路增强肝癌细胞的放疗敏感性。Objective： To investigate the effects of vitexin glucolone（ VG） on the radiosensitivity of a human hepatocelluar carcinoma cell（ HCC） line. Methods： Huh7 cells were treated with VG with or without X-radiation. Cell viability was calculated by CCK8 assay. Flow cytometry was performed for apoptosis and Western blot for the expressions of protein. Subsequently,cells were transferred with TAK1 siRNA,cell viability and apoptosis were measured. Results： VG decreased the viability of Huh7 cells in a dose-dependent manner and the inhibited effects of VG was more strengthen than radiotherapy in concentrations of 20 μmol/L and 40 μmol/L. Meanwhile,VG sensitized HCC exposed to radiation therapy to apoptosis as demonstrated by increased Bax/Bcl-2 ratio. In addition,VG enhanced the promotive effects of X-radiation on the expressions of TAK1,AMPKα1 and PPARγ. Furthermore,silence the expression of TAK1 partly reversed the effects of VG on HCC and radiosensitivity of HCC. Conclusion： VG enhances radiosensitivity of HCC via TAK1/AMPK pathway.

关 键 词：牡荆葡基黄酮 肝癌 放疗 细胞凋亡 

分 类 号：R735.7[医药卫生—肿瘤]