低浓度紫杉醇通过上调Bim表达诱导HepG2细胞凋亡

摘要

目的 探讨低浓度紫杉醇诱导肝癌细胞HepG2凋亡的机制.方法 采用MTT还原法检测细胞增殖;采用流式细胞术分析细胞凋亡与细胞周期;采用免疫印迹技术检测细胞内Bim等凋亡相关信号分子的表达.结果 紫杉醇对HepG2细胞90%的抑制浓度为9.50 nmol/L;3,6和12 nmol/L的PTX分别可诱导6.1±2.3%,17.2±4.1%和6.9±2.9%发生凋亡.3-12 nmol/L紫杉醇对Bcl-2和Bax表达无影响,但细胞内促凋亡分子Bim表达增加,同时促进Bim降解的Erk1/2磷酸化(活化相关位点)下降.结论 低浓度紫杉醇通过上调Bim表达诱导HepG2细胞凋亡.%Objective To invcstigagc the mechanism of lower conccrtratration of paclitaxcl(PTX) induced apoptosis in liver cancer HcpG2 cells. Methods Tumor cells proliferation was dctcrminicd by MTT reduction assay. Cell cycle and apoptosis were analysis by flow cytomctry . The expression of apoptosis signaling associated molecules including Bim was investigated by western blotting. Results It was found the concentration of PTX to inhibited 90% HcpG2 cell (IC90) was about 9. 50 nmoi/L. PTX( 3 to 12 nmoi/L) did not affactcd the expression of Bci-2 or Bax. But,lower concentration of PTX up-regulated the cxression apoptosis inducing molecule Bim and phosphraiatcd Erkl/2 which would promoting degradation of Bim. Conclusion Low concentration of PTX induced HcG2 cells apoptosis through up-regulating Bim expression.