| 颜宇龙,万丹婷,周洁,朱子豪,邓蒸蒸,黄波.KU60019抑制ATM对HepG2细胞辐射旁效应的调控.[J].中南医学科学杂志.,2022,(3):327-330. |
| KU60019抑制ATM对HepG2细胞辐射旁效应的调控 |
| The regulation of KU60019 inhibiting ATM on radiation-induced bystander effects in HepG2 cells |
| 投稿时间：2021-10-16 修订日期：2022-03-05 |
| DOI：10.15972/j.cnki.43-1509/r.2022.03.004 |
| 中文关键词: 共济失调毛细血管扩张症突变 ATM抑制剂KU60019 辐射旁效应 HepG2细胞 |
| 英文关键词:ataxia-telangiectasia mutated ATM inhibitor KU60019 radiation-induced bystander effects HepG2 cell |
| 基金项目:国家自然科学基金项目(81272994)；湖南省教育厅科学研究重点项目(19A429)；湖南省自然科学基金面上项目(2021JJ30592) 作者简介:颜宇龙,硕士研究生,研究方向为放射医学,E-mail为1428526055@qq.com。通信作者黄波,博士,教授,硕士研究生导师,研究方向为放射医学,E-mail为huangbo0930@163.com。 |
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| 中文摘要: |
| 目的探讨KU60019抑制ATM对HepG2细胞辐射旁效应的调控作用。方法使用KU60019抑制ATM,通过转移辐射条件刺激液构建HepG2细胞辐射旁效应模型。实验分为空白组(NC组)、辐射旁效应组(ICM组)、辐射旁效应＋KU60019组(联合组)、单纯辐照组(IR组)。MTT法检测细胞存活率；生长曲线实验检测细胞增殖；微板法检测细胞内超氧化物歧化酶(SOD)活力、丙二醛(MDA)含量；活性氧试剂盒检测细胞内活性氧(ROS)水平；荧光分光光度法检测细胞线粒体膜电位(MMP)；流式细胞术检测细胞凋亡率。结果随着KU60019浓度增加,HepG2细胞数量逐渐减少,后续选择7 μmol/L KU60019进行实验。与NC组比较,ICM组、联合组与IR组的细胞存活率、增殖能力、SOD活力、线粒体的膜电位逐渐降低(P＜0.05),细胞凋亡率、ROS与MDA含量逐渐升高(P＜0.05)。结论KU60019抑制ATM能降低HepG2细胞抗氧化能力,提高辐射敏感性。 |
| 英文摘要: |
| To investigate the regulation of KU60019 inhibiting ATM on radiation-induced bystander effects in HepG2 cells. MethodsATM protein kinase was inhibited by KU60019, and the radiation-induced bystander effect model was constructed by transferring radiative conditioned stimulation fluid to HepG2 cells. The experiment was divided into NC group (NC group), radiation-induced bystander effect group (ICM group), radiation-induced bystander effect +KU60019 group (combined group) and simple irradiation group (IR group). Cell viability was detected by MTT assay.Cell proliferation was detected by growth curve experiment. The viability of superoxide dismutase(SOD)and malondialdehyde content (MDA) in cells were detected by microplate method. The levels of reactive oxygen species (ROS) was detected by ROS kit. Mitochondrial membrane potential(MMP) was detected by fluorescence spectrophotometry. Apoptosis was detected by flow cytometry. ResultsAs the concentration of KU60019 increased, the number of HepG2 cells gradually decreased, and 7 μmol/L KU60019 concentration was selected for subsequent experiments. Compared with NC group, the cell survival rate, proliferative capacity, SOD activity and mitochondrial membrane potential of ICM group, combined group and IR group decreased gradually (P＜0.05). The cell apoptosis rate, ROS and MDA content increased gradually (P＜0.05). ConclusionInhibition of ATM by KU60019 decreased the antioxidant capacity of HepG2 cells and increased the radiation sensitivity. |
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