125I放射性粒子持续照射抑制HepG2肝癌细胞增殖的作用机制

次旦旺久; 畅智慧; 赵相轩; 林坤; 张强; 卢再鸣; 王晓明

doi:10.3969/j.issn.1001-5256.2016.10.019

125I放射性粒子持续照射抑制HepG2肝癌细胞增殖的作用机制

DOI: 10.3969/j.issn.1001-5256.2016.10.019

1. 中国医科大学附属盛京医院放射科
2. 西藏自治区人民医院放射科

基金项目:

国家自然科学基金(31371425)；盛京自由研究者基金(200802)；

详细信息

中图分类号: R735.7;R730.55
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出版历程
- 出版日期: 2016-10-20

Effect of continuous irradiation with ~(125)I radioactive seeds in inhibiting HepG2 cell proliferation and related mechanisms

Department of Radiology, Shengjing Hospital of China Medical University

Research funding:

摘要

摘要:
目的探讨125I放射性粒子持续照射抑制HepG2人肝癌细胞增殖的作用及诱导凋亡的可能潜在机制。方法以HepG2人肝癌细胞为研究对象,用125I放射性粒子体外照射装置进行持续照射。初始剂量率为5.32 c Gy/h,分别给予0、2及4 Gy照射。通过光镜及Hoechst33258染色观察形态学改变;采用克隆形成实验计算克隆形成率;利用划痕实验检测细胞迁移能力的变化;用流式细胞仪检测细胞凋亡情况。用Western Blot法检测凋亡相关蛋白表达。2组间比较采用独立样本t检验,多组间比较采用方差分析,进一步两两比较采用LSD-t检验。结果经0、2、4 Gy125I放射性粒子照射HepG2细胞后,用光学显微镜发现4 Gy组细胞密度减少,球形游离死亡细胞数目增多;经Hoechst33258染色后发现4 Gy组可见核固缩、碎裂及边集等凋亡细胞的典型特征。克隆形成实验发现对照组、2Gy组和4Gy组的克隆形成数分别为（120.00±3.61）%、（112.00±2.00）%、（45.00±3.61）%,3组比较差异有统计学意义（F=50...
- 肝肿瘤,实验性 /
- 125I放射性粒子 /
- 放射治疗剂量 /
- 细胞增殖
Abstract:
Objective To investigate the effect of continuous irradiation with~(125)I radioactive seeds in inhibiting HepG2 cell proliferation and possible mechanisms in inducing apoptosis. Methods Human hepatoma cell line HepG2 was selected as the research object and exposed to continuous irradiation with~(125)I radioactive seeds. The initial dose rate was 5. 32 c Gy / h,and HepG2 cells were exposed to a dose of 0,2,or4 Gy. A light microscope and Hoechst33258 staining were used to observe the morphological change of HepG2 cells,the colony-forming assay was used to calculate plating efficiency,the scratch test was used to evaluate the change in migration ability,flow cytometry was used to measure cell apoptosis,and Western Blot was used to measure the expression of apoptosis-related proteins. An analysis of variance was used for comparison between multiple groups,and the least significant difference method was used for further comparison between any two groups. Results After HepG2 cells were exposed to~(125)I radioactive seeds at a dose of 0 Gy,2 Gy,or 4 Gy,the 4 Gy group showed a reduction in cell density and an increase in the number of spherical free dead cells,as was shown by the light microscope; Hoechst33258 staining showed that the 4 Gy group had typical features of apoptotic cells,such as karyopyknosis,fragmentation,and margination. The colony-forming assay showed that there were significant differences in plating efficiency between the control group,2 Gy group,and 4 Gy group( 120. 00% ± 3. 61%,112. 00% ± 2. 00%,and 45. 00% ± 3. 61%,F = 508. 90,P < 0. 001). The scratch test showed that there were significant differences in cell migration rate between the control group,2 Gy group,and 4 Gy group( 21. 24% ± 4. 36%,19. 93% ± 3. 37%,and 11. 42% ± 0. 65%,F = 8. 29,P < 0. 001). The results of flow cytometry for cell apoptosis showed that there were significant differences in cell apoptosis rate between the control group,2 Gy group,and 4 Gy group( 4. 33% ± 0. 67%,6. 90% ± 1. 31%,and 17. 03% ±1. 43%,F = 110. 01,P < 0. 001). Western blot showed that ~(125)I irradiation significantly inhibited the expression of tumor proliferation-related protein PCNA,apoptosis-related protein Survivin,and Bcl-2 and promoted the expression of pro-apoptotic proteins Bak and Bax. Conclusion~(125)I radioactive seeds inhibit the growth of HepG2 cells through promoting HepG2 cell apoptosis and inhibiting proliferation and migration. The possible mechanism may be related to the inhibition of the expression of apoptosis-related proteins.
- liver neoplasms /
- experiment /
- 125I seeds /
- radiotherapy dosage

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