| 姜玉良,刘敬佳,李金娜,王皓,曲昂,赵勇,王俊杰.125I粒子持续低剂量率照射对人喉癌细胞系Hep-2的抑制作用[J].中华放射医学与防护杂志,2013,33(6):593-596 |
| 125I粒子持续低剂量率照射对人喉癌细胞系Hep-2的抑制作用 |
| The inhibition effect of continuous low dose rate radiation by 125I radioactive seeds on Hep-2 larynx cancer cell line |
| 投稿时间：2013-03-25 |
| DOI：10.3760/cma.j.issn.0254-5098.2013.06.006 |
| 中文关键词: 放射敏感性 DNA损伤修复 细胞凋亡 G2/M期阻滞 |
| 英文关键词:Radiosensitivity DNA damage repair Cell apoptosis G2/M arrest |
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| 中文摘要: |
| 目的 探讨125I粒子持续低剂量率照射对人喉癌细胞Hep-2的抑制作用及其机制。方法 实验分为空白对照组、X射线单次高剂量率照射组（SDR组）、125I粒子持续低剂量率照射组（125I-CLDR组）。克隆形成实验检测Hep-2细胞在两种照射方式下的放射敏感性，并计算125I-CLDR的相对生物学效应。锥虫蓝染色计数两种照射方式下Hep-2细胞的增殖情况。流式细胞仪检测细胞凋亡和细胞周期阻滞情况。Western blot检测细胞内总γ-H2AX的表达水平。结果 Hep-2细胞对125I-CLDR的放射敏感性高于SDR，125I-CLDR相对生物学效应约为1.61，且α/β比值高于SDR。SDR和125I-CLDR均能抑制Hep-2细胞增殖（t=30.9、40.7，P<0.05），且后者的抑制作用更为明显（t=9.8，P<0.05）。125I-CLDR诱导细胞凋亡和G2/M期细胞阻滞的效应强于SDR（t=5.8、19.8， P<0.05）。结论 125I-CLDR对Hep-2细胞的抑制作用高于SDR，主要机制是降低Hep-2细胞的DNA损伤修复能力，促进细胞死亡；诱导细胞凋亡和G2/M期阻滞，抑制细胞再增殖。 |
| 英文摘要: |
| Objective To investigate the inhibition effect of continuous low dose rate radiation by125I radioactive seeds on Hep-2 cells and the corresponding mechanisms. Methods Hep-2 cells were divided into three groups, control group, single dose radiation group with high dose rate form X-rays (SDR) and continuous low dose rate radiation by 125I seeds group (125I-CLDR). After exposure to SDR and 125I-CLDR, colony formation assay was used to determine the radiosensitivity and RBE, trypan blue exclusion assay was used to determine cell proliferation, and flow cytometry was used to detect cell apoptosis and cell cycle arrest. Results The radiosensitivity of Hep-2 cells to 125I-CLDR was higher than that to SDR. The RBE of 125I-CLDR versus SDR was approximately 1.61. The α/β ratio of 125I-CLDR group was higher than that of SDR group. Both SDR and 125I-CLDR inhibited cell proliferation (t=30.9,40.7, P<0.05), in which 125I-CLDR was stronger than SDR (t=9.8, P<0.05). In addition, the incidences of apoptosis and G2/M arrest induced by 125I-CLDR were also stronger than those induced by SDR (t=5.8,19.8,P<0.05). Conclusions 125I-CLDR generates more serious inhibition effects than SDR on reducing cellular DNA repair capacity, inducing cell apoptosis and G2/M arrest and inhibiting proliferation of Hep-2 cells. |
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