罗格列酮对HT29、HCT116结肠癌细胞凋亡影响及机制探究

发布时间：2018-09-01 19:24

【摘要】：目的探讨罗格列酮对结肠癌HT29、HCT116细胞增殖、凋亡情况的影响以及AKT/GSK3β信号通路的变化。方法 HT29、HCT116结肠癌细胞经不同浓度罗格列酮(20.0μmol/L,40.0μmol/L,80.0μmol/L)处理后,采用MTT法检测细胞增殖能力的变化,annexin-V FITC/PI试剂盒检测细胞凋亡情况,Western blot检测Bcl2、Bax以及Akt、GSK3β表达情况。结果与空白对照组相比,不同浓度的罗格列酮对HT29、HCT116结肠癌细胞的增殖均有影响(P0.01),并且影响呈剂量依赖关系;不同浓度的罗格列酮对HT29、HCT116细胞均有诱导凋亡的作用(P0.01),且诱导HT29、HCT116细胞凋亡呈剂量依赖性;罗格列酮处理细胞48 h后,与空白对照组相比Bcl2/Bax表达水平、P-GSK3β、P-Akt表达水平明显下降(P0.01),Akt、GSK3β表达水平较空白对照组差异无显著性(P0.05)。结论罗格列酮可能通过抑制Akt/GSK3β通路的激活,改变Bcl2/Bax情况,发挥抑制细胞增殖、诱导凋亡的作用。
[Abstract]:Objective To investigate the effects of rosiglitazone on proliferation and apoptosis of colon cancer cells HT29 and HCT116 and the changes of AKT/GSK3 beta signaling pathway.Methods HT29 and HCT116 colon cancer cells were treated with rosiglitazone at different concentrations (20.0, 40.0 and 80.0 micromol/L). Results Compared with the blank control group, different concentrations of rosiglitazone had effect on the proliferation of HT29 and HCT116 colon cancer cells (P 0.01), and the effect was dose-dependent; different concentrations of rosiglitazone could induce apoptosis of HT29 and HCT116 cells. The expression of Bcl 2/Bax, P-GSK 3 beta, P-Akt decreased significantly after rosiglitazone treatment for 48 hours compared with the control group (P 0.01). The expression of Akt, GSK 3 beta had no significant difference compared with the blank control group (P 0.05). Conclusion Rosiglitazone may inhibit the expression of Akt/GSK 3 beta. Activation of the beta pathway can alter Bcl2/Bax and inhibit cell proliferation and induce apoptosis.
【作者单位】：华北理工大学附属医院;华北理工大学临床医学院;
【基金】：2017年政府资助省级临床医学优秀人才项目中国煤炭工业协会2017年度科学技术研究指导性计划项目(MTKJ2017-331)
【分类号】：R735.35

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