中华放射医学与防护杂志
中華放射醫學與防護雜誌
중화방사의학여방호잡지
Chinese Journal of Radiological Medicine and Protection
2013年
3期
256-260
,共5页
叶爽%袁德晓%谢月霞%潘燕%邵春林
葉爽%袁德曉%謝月霞%潘燕%邵春林
협상%원덕효%사월하%반연%소춘림
低剂量辐射%细胞增殖%辐射敏感性%凋亡%基因表达
低劑量輻射%細胞增殖%輻射敏感性%凋亡%基因錶達
저제량복사%세포증식%복사민감성%조망%기인표체
Low-dose-radiation%Cell proliferation%Radiosensitivity%Apoptosis%Gene expressions
目的 探讨长期低剂量(LDR)γ辐射对人B淋巴母细胞HMy2.CIR(HMy)辐射敏感性的影响及其机制.方法 实验将HMy细胞分为对照组和长期LDR组,其中长期LDR组选用可以显著促进细胞增殖的低剂量γ射线对HMy细胞每周照射3次,每次0.032 Gy,连续照射4周,在长期LDR处理结束后分别对部分对照组和长期LDR组细胞进行2 Gy照射.以CCK-8[内含WST-8,即2-(2-甲氧基-4-硝基苯基)-3-(4-硝基苯基)-5-(2,4-二磺酸苯)-2H-四唑单钠盐]法检测细胞增殖和辐射敏感性,流式细胞术检测细胞凋亡率和γ-H2AX表达,RT-PCR法检测细胞周期相关基因cyclinD1、细胞增殖核抗原PCNA,以及凋亡相关基因bcl-2和bax的表达.结果 长期LDR可以显著提高细胞的增殖率(t =9.607,P＜0.01),增加cyclinD1和PCNA基因表达(t=6.869、9.229,P＜0.01),增加抗凋亡基因bcl-2表达(t=2.662,P＜0.05),降低抑凋亡基因bax的表达(t=19.908,P＜0.01).同时,受长期LDR照射的细胞对攻击剂量(2 Gy)产生适应性,使得细胞辐射敏感性显著降低(t =8.896,P＜0.01)；与单纯2 Gy照射组相比,LDR+2 Gy组细胞γ-H2AX表达量(=10.264,P＜0.01)和细胞凋亡率(t=4.762,P＜0.01)均显著降低.结论 长期LDR辐射可通过促进周期相关基因表达从而促进细胞增殖,并通过减少细胞凋亡来降低其辐射敏感性.
目的 探討長期低劑量(LDR)γ輻射對人B淋巴母細胞HMy2.CIR(HMy)輻射敏感性的影響及其機製.方法 實驗將HMy細胞分為對照組和長期LDR組,其中長期LDR組選用可以顯著促進細胞增殖的低劑量γ射線對HMy細胞每週照射3次,每次0.032 Gy,連續照射4週,在長期LDR處理結束後分彆對部分對照組和長期LDR組細胞進行2 Gy照射.以CCK-8[內含WST-8,即2-(2-甲氧基-4-硝基苯基)-3-(4-硝基苯基)-5-(2,4-二磺痠苯)-2H-四唑單鈉鹽]法檢測細胞增殖和輻射敏感性,流式細胞術檢測細胞凋亡率和γ-H2AX錶達,RT-PCR法檢測細胞週期相關基因cyclinD1、細胞增殖覈抗原PCNA,以及凋亡相關基因bcl-2和bax的錶達.結果 長期LDR可以顯著提高細胞的增殖率(t =9.607,P＜0.01),增加cyclinD1和PCNA基因錶達(t=6.869、9.229,P＜0.01),增加抗凋亡基因bcl-2錶達(t=2.662,P＜0.05),降低抑凋亡基因bax的錶達(t=19.908,P＜0.01).同時,受長期LDR照射的細胞對攻擊劑量(2 Gy)產生適應性,使得細胞輻射敏感性顯著降低(t =8.896,P＜0.01)；與單純2 Gy照射組相比,LDR+2 Gy組細胞γ-H2AX錶達量(=10.264,P＜0.01)和細胞凋亡率(t=4.762,P＜0.01)均顯著降低.結論 長期LDR輻射可通過促進週期相關基因錶達從而促進細胞增殖,併通過減少細胞凋亡來降低其輻射敏感性.
목적 탐토장기저제량(LDR)γ복사대인B림파모세포HMy2.CIR(HMy)복사민감성적영향급기궤제.방법 실험장HMy세포분위대조조화장기LDR조,기중장기LDR조선용가이현저촉진세포증식적저제량γ사선대HMy세포매주조사3차,매차0.032 Gy,련속조사4주,재장기LDR처리결속후분별대부분대조조화장기LDR조세포진행2 Gy조사.이CCK-8[내함WST-8,즉2-(2-갑양기-4-초기분기)-3-(4-초기분기)-5-(2,4-이광산분)-2H-사서단납염]법검측세포증식화복사민감성,류식세포술검측세포조망솔화γ-H2AX표체,RT-PCR법검측세포주기상관기인cyclinD1、세포증식핵항원PCNA,이급조망상관기인bcl-2화bax적표체.결과 장기LDR가이현저제고세포적증식솔(t =9.607,P＜0.01),증가cyclinD1화PCNA기인표체(t=6.869、9.229,P＜0.01),증가항조망기인bcl-2표체(t=2.662,P＜0.05),강저억조망기인bax적표체(t=19.908,P＜0.01).동시,수장기LDR조사적세포대공격제량(2 Gy)산생괄응성,사득세포복사민감성현저강저(t =8.896,P＜0.01)；여단순2 Gy조사조상비,LDR+2 Gy조세포γ-H2AX표체량(=10.264,P＜0.01)화세포조망솔(t=4.762,P＜0.01)균현저강저.결론 장기LDR복사가통과촉진주기상관기인표체종이촉진세포증식,병통과감소세포조망래강저기복사민감성.
Objective To investigate the effects of long-term low-dose radiation (LDR) of γ-rays on the proliferation and radiosensitivity of human lymphoblast cells HMy2.CIR (HMy) and to elucidate the underlying mechanism.Methods HMy cells were divided into control group and long-term LDR group.For the long-term LDR treatment,HMy cells were fractionally exposed to a low dose of γ-rays,which could enhance cell proliferation,3 times per week for 4 weeks.After the long-term LDR exposure,part of the control and long-term LDR exposed cells were further irradiated with a challenging dose (2 Gy) of γ-rays.Then cell proliferation and radiosensitivity were assayed by CCK-8 kit,cell apoptosis,and γ-H2AX formation was measured by flow cytometry.Gene expressions of cyclinD1,PCNA,bcl-2 and bax were detected by RT-PCR.Results The long-term LDR significantly increased cell proliferation (t =9.607,P ＜ 0.01) accompanied with up-regulation of cell cycle regulation gene cyclinD1 (t =6.869,P ＜ 0.01),proliferation regulation gene PCNA (proliferating cell nuclear antigen) (t =9.229,P ＜ 0.01) and bcl-2 gene (t =2.662,P ＜ 0.05),but decreased the expression of pro-apoptotic gene bax (t =19.908,P ＜0.01) in HMy cells.Compared to untreated cells,the long-term LDR decreased cell radiosensitivity (t =8.896,P ＜ 0.01),including apoptosis induction (t =4.762,P ＜ 0.01) and γ-H2AX formation (t =10.264,P＜0.01).Conclusions The long-term LDR promoted cell proliferation by up-regulating cell cycle related genes,while it reduced the radiosensitivity of HMy cells with acquisition of apoptotic resistance.
