漆树黄酮逆转人肝癌细胞HepG2上皮间质转化的实验研究  

Effect of fisetin on epithelial-mesenchymal transition in hepatocellular carcinoma cell line HepG2

作　　者：李蓉[1] 黎小兵[1] 敬敏[2] 陈锦[1] 黄培春[1] 

机构地区：[1]广东医学院病理生理学教研室,广东湛江524023 [2]广东医学院病理学教研室,广东湛江524023

出　　处：《中国药理学通报》2011年第1期91-95,共5页Chinese Pharmacological Bulletin

基　　金：广东省教育厅重点学科建设基金(NoGX9404)

摘　　要：目的研究漆树黄酮对人肝癌细胞HepG2上皮间质转化的影响及其可能机制。方法用不同浓度的漆树黄酮(50、100、200μmol.L-1)处理HepG2细胞;MTT法检测漆树黄酮对HepG2细胞的细胞毒作用;用Transwell小室法检测漆树黄酮对HepG2细胞侵袭能力和趋化运动能力的影响,RT-PCR法检测p38MAPK、E-cadherin和vimentin mRNA表达,Western blot检测p38MAPK、E-cadherin和vimentin蛋白表达。结果漆树黄酮作用细胞24 h后能抑制HepG2细胞体外趋化运动和侵袭能力。漆树黄酮能引起HepG2细胞形态学的变化,能降低p38 MAPK和vimentin mRNA和蛋白表达,但不能改变E-Cadherin的表达。结论漆树黄酮能逆转人肝癌细胞HepG2的上皮间质转化,其抗肿瘤侵袭运动的机制可能与抑制p38MAPK的表达有关。Aim To investigate the effect of fisetin on epithelial-mesenchymal transition in hepatoma cell line HepG2 and its possible mechanism.Methods HepG2 cell were treated with fisetin（50,100,200 μmol·L-1）;MTT assay was used to examine the cytotoxicity of fisetin in HepG2 cells;Transwell Chamber assay was performed to determine the effect on invasion and migratory capacity of the cells by fisetin;The mRNA expression of p38MAPK,E-cadherin,vimentin was determined by RT-PCR,and the protein expression of p38MAPK,E-cadherin,vimentin was detected by Western blotting.Results Fisetin inhibited migration and invasion capacity of HepG2 cells in vitro.The morphologic changes had been observed by the treatment of fisetin.The mRNA expression and the protein expression of p38MAPK and vimentin in HepG2 cells were also decreased by the treatment of fisetin,but those of E-cadherin manifest no change.Conclusion The characteristic morphology and molecular changes of EMT was reversed by fisetin and its possible anti-invasion and anti-migration mechanism was associated with downregulation of p38MAPK in HepG2.

关 键 词：漆树黄酮 肝癌 上皮间质转化 P38MAPK 侵袭 运动 

分 类 号：R284.1[医药卫生—中药学] R329.24[医药卫生—中医学]