紫花前胡苷通过调控CXCL5-ERK/MEK信号轴发挥抗肝癌作用  

Nodakenin exerts anti-hepatocellular carcinoma effects by regulating CXCL5-ERK/MEK signal axis

作　　者：王鹏利 王国泰 闫曙光 李京涛 罗璐 白垚 周小燕 WANG Peng-li;WANG Guo-tai;YAN Shu-guang;LI Jing-tao;LUO Lu;BAI Yao;ZHOU Xiao-yan(Affiliated Hospital of Shaanxi University of Traditional Chinese Medicine,Xianyang 712000,China)

机构地区：[1]陕西中医药大学附属医院,咸阳712000

出　　处：《天然产物研究与开发》2022年第6期1014-1020,共7页Natural Product Research and Development

基　　金：咸阳市2019年重点研发计划(2019k02-100)。

摘　　要：本文探讨紫花前胡苷(nodakenin,NK)对肝癌细胞的作用及机制。不同浓度紫花前胡苷处理HepG2和MHCC-97H细胞,CCK-8检测细胞增殖变化,细胞划痕和Trans-wells实验观察细胞迁移和侵袭能力变化。紫花前胡苷能够显著抑制HepG2和MHCC-97H细胞增殖、体外迁移和侵袭;RNA-seq分析紫花前胡苷给药前后各基因表达,qRT-PCR、Western blotting和细胞免疫荧光进行验证分析,结果表明紫花前胡苷给药后趋化因子5(CXCL5)的表达显著降低,同时ERK和MEK磷酸化被抑制。综上所述紫花前胡苷通过下调CXCL5抑制ERK/MEK信号通路从而发挥抗肝癌作用。This paper investigates the effect and mechanism of nodakenin(NK)on hepatocellular carcinoma cells.HepG2 and MHCC-97 H cells were treated with different concentrations of NK.Cell proliferations were detected by CCK-8,and migration and invasion abilities were observed by cell scratch and Trans-wells experiments.NK significantly inhibited the proliferation,migration and invasion of HepG2 and MHCC-97 H cells in vitro.RNA-seq was conducted to analyze the expression of each gene before and after the administration of NK.qRT-PCR,Western blotting and cellular immunofluorescence were used to verify the RNA-seq result.The results showed that the expression of chemokine 5(CXCL5)was significantly decreased after administration of NK,and the phosphorylation of ERK and MEK was inhibited at the same time.In summary,it can be concluded that NK inhibits ERK/MEK signaling pathway by down-regulating CXCL5,thereby inhibiting hepatocellular carcinoma.

关 键 词：紫花前胡苷 CXCL5 ERK/MEK 肝癌 

分 类 号：R932[医药卫生—生药学]