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临床输血与检验

临床输血与检验 ›› 2017, Vol. 19 ›› Issue (6): 540-542.DOI: 10.3969/j.issn.1671-2587.2017.06.002

• 基础实验 • 上一篇    下一篇

雷公藤甲素诱导急性髓细胞白血病干细胞凋亡及其机制*

郑维威, 吕长坤, 张文静   

  1. 230000 合肥,安徽医科大学附属省立医院检验科（郑维威,张文静）;
    商丘医学高等专科学校医学技术系（吕长坤）
  • 收稿日期:2017-06-25 出版日期:2017-12-20 发布日期:2017-12-13
  • 作者简介:郑维威（1984-）,男,安徽凤阳人,主管技师,博士,主要从事临床医学检验及临床血液学研究,（E-mail）379667349@qq.com。
  • 基金资助:
    *本课题受国家自然科学基金项目（No.81700154）资助

Mechanism of Triptolide Induced Apoptosis of Acute Myelogenous Leukemia Stem Cells

ZHENG WEI-wei, LV CHANG-kun, ZHANG WEN-jing   

  1. Dept.of Laboratory Medicine,Affiliated Anhui Provincial Hospital,Anhui Medical University,Hefei,Anhui 230000
  • Received:2017-06-25 Online:2017-12-20 Published:2017-12-13

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摘要： 目的 探讨雷公藤甲素诱导急性髓细胞白血病干细胞凋亡的分子机制。方法 采用MTT法检测雷公藤甲素对KG-1细胞的增殖抑制作用,计算出IC50值,按照浓度梯度用雷公藤甲素处理KG-1细胞48 h,流式细胞仪检测细胞凋亡变化。Western blot法检测Bcl-2、β-catenin、p-AKT和AKT 等蛋白的变化。结果 雷公藤甲素对KG-1细胞的增殖抑制呈剂量依赖性,IC50值约为4 nmmol/L,其还可诱导KG-1细胞凋亡。雷公藤甲素能够下调Bcl-2、β-catenin,p-AKT等蛋白的表达水平。结论 雷公藤甲素诱导KG-1细胞的分子机制可能与Bcl-2、β-catenin、p-AKT的下调有关。

关键词: 雷公藤甲素, 髓细胞白血病干细胞, 凋亡

Abstract: Objective To study the molecular mechanisms of acute myelogenous leukemia stem cell apoptosis induced by triptolide. Methods Proliferation inhibition of triptolide to KG-1 cell was determined by MTT, IC50 concentration was calculated. According to the concentration gradient of triptolide, KG-1cells were collected to detect cell apoptosis via flow cytometry 48h after treatment. Bcl-2, beta-catenin, p-AKT and AKT proteins were detected by Western blot. Results Triptolide to KG-1 cell proliferation inhibition is in dose dependent manner and IC50 is about 4 nmmol/L, it can also induce apoptosis of KG-1 cell. Bcl-2, beta-catenin, p-AKT proteins can be down-regulated by triptolide. Conclusions Molecular mechanism of triptolide induced KG - 1 cell may be related to the Bcl-2, beta-catenin and p-AKT.

Key words: Triptolide, Myeloid leukemia stem cell, Apoptosis

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