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作 者:庄洪卿[1] 王俊杰[2] 赵勇[3] 王济东[2] 廖安燕[2]
机构地区:[1]天津医科大学附属天津市肿瘤医院放射治疗科 [2]北京大学第三医院肿瘤治疗中心放射治疗科,100083 [3]中国科学院动物研究所生物膜膜生物国家重点实验室
出 处:《中华放射医学与防护杂志》2008年第2期-,共4页Chinese Journal of Radiological Medicine and Protection
摘 要:目的 探讨125I粒子持续性低剂量率照射下肿瘤细胞的凋亡和周期改变.方法 采用CL187人结肠癌细胞系体外培养,分为空白对照组、60Co单次高剂量率照射组、125I低剂量率照射组.单次高剂量率组以2 Gy/min给予细胞1、2、4、6、8和10 Gy的照射,低剂量率组以2.77 cGy/h的初始剂量率给予相同剂量照射,照射后24 h根据肿瘤细胞死亡率和14 d克隆形成率评价不同照射方式对肿瘤细胞的杀伤效果.同时,用放射性125I粒子以2.77 cGy/h的剂量率,给予细胞2、5和10 Gy的照射,应用流式细胞术测量其凋亡和细胞周期的变化.结果 低剂量率组照射后细胞死亡率在1 Gy时低于60Co单次高剂量率组,随着剂量的上升,2 Gy后,超过单次高剂量率组,但整体上125I粒子照射后细胞死亡率高于60Co组(P=0.011).125I持续性低剂量率照射组的克隆增殖率明显低于60Co单次高剂量率组(P=0.0021).低剂量率照射下,2 Gy时仅能引起G2/M期阻滞和凋亡,5 Gy时达到峰值,10 Gy时细胞周期阻滞和凋亡的比率依然很高,但相对于5 Gy有所下降;同时G2/M期阻滞和凋亡变化呈现出相同的趋势.结论 在相同剂量条件下,125I粒子持续照射低剂量率照射比60Co单次高剂量照射对CL187肿瘤细胞具有更强的杀伤效应;G2/M期阻滞引起的凋亡是低剂量率照射杀伤肿瘤细胞的主要机制.Objective To study the response patterns of CL187 cell lines irradiated with low dose rates of 125I seeds.Methods CL187 cells were exposed with radioactive.125I seeds and 60Co source,which were put under culture plate.The radiation response at different doses and dose-rates were evaluated through cell-proliferation assessed by the colony-forming assay and death rate after irradiation.Meanwhile,cell cycle arrest and apoptosis were measured by flow cytometry after 2,5 and 10 Gy of low dose rate irradiation.Remits It was shown that the cell-killing effects were related to the doses and dose-rates.At 1 Gy,comparison of the death rate between the low and high dose rate showed that the higher dose rate led to increased cell responses,but at the doses higher than 2 Gy,the effect of the low dose rate were more efficient.At the same dose,the survival fraction of 125I was always lower than that of 60Co.Exposed to the low dose rate irradiation,apoptosis and G2/M cell cycle arrest rose a little at 2 Gy,the peak appeared at 5 Gy,and the ratio at 10 Gy Was also high but lower than at 5 Gy.Furthermore,the G2/M cell cycle arrest and apoptosis changed together along with the doses.Conclusions At the same dose,125I seeds have more cell-killing effects than 60Co at high dose rate irradiation.Apoptosis following the G2/M cell cycle arrest were the main mechanism of cell-killing effects under low dose rate irradiation.
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