CAJ | 학술논문

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(=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.
목적 탐토125Ⅰ입자지속저제량솔조사대인후암세포Hep-2적억제작용급기궤제.방법 실험분위공백대조조、X사선단차고제량솔조사조(SDR조)、125Ⅰ입자지속저제량솔조사조(125Ⅰ-CLDR조).극륭형성실험검측Hep-2세포재량충조사방식하적방사민감성,병계산125Ⅰ-CLDR적상대생물학효응.추충람염색계수량충조사방식하Hep-2세포적증식정황.류식세포의검측세포조망화세포주기조체정황.Western blot검측세포내총γ-H2AX적표체수평.결과 Hep-2세포대125Ⅰ-CLDR적방사민감성고우SDR,125Ⅰ-CLDR상대생물학효응약위1.61,차α/β비치고우SDR.SDR화125Ⅰ-CLDR균능억제Hep-2세포증식(=30.9、40.7,P＜0.05),차후자적억제작용경위명현(t=9.8,P＜0.05).125Ⅰ-CLDR유도세포조망화G2/M기세포조체적효응강우SDR(t =5.8、19.8,P＜0.05).결론 125Ⅰ-CLDR대Hep-2세포적억제작용고우SDR,주요궤제시강저Hep-2세포적DNA손상수복능력,촉진세포사망;유도세포조망화G2/M기조체,억제세포재증식.
Objective To investigate the inhibition effect of continuous low dose rate radiation by 125Ⅰ 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 by125Ⅰ-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.