香蜂草苷诱导人肝癌细胞株HepG2凋亡及其作用机制  

Apoptosis-inducing Effect of Didymin on Human Hepatoma Cell Line HepG 2 and Its Action Mechanism

作　　者：朱勋帅 林兴[1] 黄权芳[2] 林军[1] 

机构地区：[1]广西医科大学药学院,南宁530021 [2]广西中医药大学第一附属医院,南宁530023

出　　处：《天然产物研究与开发》2017年第4期579-583,共5页Natural Product Research and Development

基　　金：国家自然科学基金(81260505;81473431);广西自然科学基金(2014GXNSFAA118154)

摘　　要：为了研究香蜂草苷对肝癌细胞株HepG2凋亡的影响,并探讨其作用机制,利用MTT法检测香蜂草苷对HepG2细胞增殖的抑制作用,流式细胞术检测细胞凋亡率,试剂盒检测caspase-3和caspase-9活性,Western blot检测Bcl-2、Bax、RKIP、ERK、p-ERK蛋白表达。实验结果表明香蜂草苷可抑制HepG2细胞增殖并诱导其凋亡,其机制可能与提高caspase-3和caspase-9活性,上调Bax和下调Bcl-2表达有关。此外,我们的研究显示香蜂草苷诱导HepG2细胞凋亡可能还与其增加RKIP表达,抑制ERK/MAPK信号通路有关。To investigate the effect of didymin on apoptosis of human hepatocellular carcinoma HepG2 cells and its action mechanism. MTr assay was used to investigate the effect of didymin on proliferation of HepG2 cells. Flow cytometry as- say was used to analyze apoptosis rate of HepG2 cells. The effects of didymin on caspase-3 and caspase-9 activities were detected using available kits. The protein expressions of Bcl-2, Bax, RKIP, ERK and p-ERK were detected by Western blot. The experimental resultsshowedthatdidymin can inhibit HepG2 proliferation and induce cell apoptosis, by activating caspase-3 and -9, regulating Bax andBcl-2 level. Moreover, our study indicated that didyminincreased RKfPexpression, resulting in the inactivation of ERK/MAPK signaling pathways.

关 键 词：香蜂草苷 HEPG2细胞 凋亡 Raf激酶抑制剂 ERK/MAPK信号通路 

分 类 号：R93[医药卫生—生药学]