癌症进展
癌癥進展
암증진전
ONCOLOGY PROGRESS
2015年
1期
69-73
,共5页
黄鹂%刘敬佳%杜立法%曲昂%赵勇%王俊杰%张建国%张杰
黃鸝%劉敬佳%杜立法%麯昂%趙勇%王俊傑%張建國%張傑
황리%류경가%두입법%곡앙%조용%왕준걸%장건국%장걸
125I粒子%低剂量率照射%Hep2细胞%DNA损伤%细胞周期
125I粒子%低劑量率照射%Hep2細胞%DNA損傷%細胞週期
125I입자%저제량솔조사%Hep2세포%DNA손상%세포주기
125I radioactive seeds%low dose rate radiation%Hep2 cells%DNA damage%cell cycle
目的：探讨125I 粒子持续低剂量率照射与分次照射、单次照射对人喉鳞癌细胞 Hep2的抑制作用及其作用机制。方法实验分为无照射对照组（Ctrl 组）、单次照射组（SDR 组）、分次照射组（FDR 组）和125I 粒子持续低剂量率照射组（125I-CLDR 组）四组。采用细胞克隆形成实验法检测 Hep2细胞在不同照射条件下细胞克隆的形成能力；用流式细胞仪检测细胞凋亡和细胞周期阻滞情况；用蛋白印迹法检测不同照射条件后 Hep2细胞总γ-H2AX、CyclinB1、Caspase3蛋白表达的变化。结果经2 Gy、4 Gy、6 Gy 的剂量照射，125I-CLDR 组 Hep2细胞克隆形成率均低于 SDR 组和 FDR 组。经4 Gy 的剂量照射后，125I-CLDR 组 Hep2细胞出现 G2/M 期阻滞，且阻滞效应较 SDR 组及 FDR 组的细胞强；125I-CLDR 组 Hep2细胞的凋亡比例明显高于 SDR 组及 FDR 组；三个照射组γ-H2AX、CyclinB1、Caspase3、NF-κB、P21和 Cdk1的表达水平上调，125I-CLDR 组 p-Cdc25c 蛋白表达水平低于 SDR 组和 FDR 组。结论在本实验条件下，125I 粒子持续低剂量率照射较单次照射、分次照射能够诱发更多 Hep2细胞出现 DNA 损伤、引起持续的 G2/M 期阻滞、诱导细胞凋亡并抑制细胞的再增殖。
目的：探討125I 粒子持續低劑量率照射與分次照射、單次照射對人喉鱗癌細胞 Hep2的抑製作用及其作用機製。方法實驗分為無照射對照組（Ctrl 組）、單次照射組（SDR 組）、分次照射組（FDR 組）和125I 粒子持續低劑量率照射組（125I-CLDR 組）四組。採用細胞剋隆形成實驗法檢測 Hep2細胞在不同照射條件下細胞剋隆的形成能力；用流式細胞儀檢測細胞凋亡和細胞週期阻滯情況；用蛋白印跡法檢測不同照射條件後 Hep2細胞總γ-H2AX、CyclinB1、Caspase3蛋白錶達的變化。結果經2 Gy、4 Gy、6 Gy 的劑量照射，125I-CLDR 組 Hep2細胞剋隆形成率均低于 SDR 組和 FDR 組。經4 Gy 的劑量照射後，125I-CLDR 組 Hep2細胞齣現 G2/M 期阻滯，且阻滯效應較 SDR 組及 FDR 組的細胞彊；125I-CLDR 組 Hep2細胞的凋亡比例明顯高于 SDR 組及 FDR 組；三箇照射組γ-H2AX、CyclinB1、Caspase3、NF-κB、P21和 Cdk1的錶達水平上調，125I-CLDR 組 p-Cdc25c 蛋白錶達水平低于 SDR 組和 FDR 組。結論在本實驗條件下，125I 粒子持續低劑量率照射較單次照射、分次照射能夠誘髮更多 Hep2細胞齣現 DNA 損傷、引起持續的 G2/M 期阻滯、誘導細胞凋亡併抑製細胞的再增殖。
목적：탐토125I 입자지속저제량솔조사여분차조사、단차조사대인후린암세포 Hep2적억제작용급기작용궤제。방법실험분위무조사대조조（Ctrl 조）、단차조사조（SDR 조）、분차조사조（FDR 조）화125I 입자지속저제량솔조사조（125I-CLDR 조）사조。채용세포극륭형성실험법검측 Hep2세포재불동조사조건하세포극륭적형성능력；용류식세포의검측세포조망화세포주기조체정황；용단백인적법검측불동조사조건후 Hep2세포총γ-H2AX、CyclinB1、Caspase3단백표체적변화。결과경2 Gy、4 Gy、6 Gy 적제량조사，125I-CLDR 조 Hep2세포극륭형성솔균저우 SDR 조화 FDR 조。경4 Gy 적제량조사후，125I-CLDR 조 Hep2세포출현 G2/M 기조체，차조체효응교 SDR 조급 FDR 조적세포강；125I-CLDR 조 Hep2세포적조망비례명현고우 SDR 조급 FDR 조；삼개조사조γ-H2AX、CyclinB1、Caspase3、NF-κB、P21화 Cdk1적표체수평상조，125I-CLDR 조 p-Cdc25c 단백표체수평저우 SDR 조화 FDR 조。결론재본실험조건하，125I 입자지속저제량솔조사교단차조사、분차조사능구유발경다 Hep2세포출현 DNA 손상、인기지속적 G2/M 기조체、유도세포조망병억제세포적재증식。
Objective To investigate the inhibition effects of different irradiation methods on the proliferation of Hep2, which is the human laryngeal squamous carcinoma cell line, and the corresponding mechanisms. Method Four groups of patients receiving different irradiations were compared in our experiment, which were non-radiation control group (Ctrl), high dose rate single dose radiation group (SDR), high dose rate fractionated dose radiation group (FDR), and iodine-125 seeds continuous low dose rate radiation group (125I-CLDR), respectively. Colony forma-tion assay was used to determine the radiosensitivity of Hep2 cells to each radiation, and flow cytometry was applied for detecting cell apoptosis and cell cycle arrest, while the protein expression levels of γ-H2AX, CyclinB1 and Cas-pase3 were detected with Western blot. Result The capability of clone formation of Hep2 cells after 2 Gy, 4 Gy, 6 Gy irradiation was lower in 125I-CLDR group compare with SDR and FDR group. After 4 Gy irradiation, 125I-CLDR induced the most significant Hep2 cells arrest effect of G2/M among the three groups. And the highest cell apoptosis proportion was seen in 125I-CLDR group either. The expression levels of γ-H2AX, CyclinB1, Caspase3, NF- κB, P21 and Cdk1 increased among three treatment groups. While p-Cdc25c expressed the least in 125I-CLDR group. Conclu-sion In the context of this study, 125I-CLDR obviously reduces cellular DNA repair capacity, induces cell apoptosis and G2/M arrest, and inhibits cell reproliferation.
