持续低剂量率照射后HepG2细胞的ATM磷酸化.pdfVIP

• 348 • 中华放射医学与防护杂志棚8 年 8 月第 28 号在第 4 期 Chin J Radiol Med Prot. August 2∞8. Vo 1.28. No.4 ·基础研究· 持续低剂量率照射后 HepG2 细胞的 ATM 磷酸化 梅在林杨建勇 学彦豪杜端明陈在中刘鹏程 I 摘要] 目的 探讨持续低剂量率照射下 HepG2 细胞共济失调毛细血管扩张症突变慕因 (ATM)磷酸化的变化规律。方法 !但用问接免疫荧光、Westem blot 技术检测持续低剂最率(8.28 cGy/h) 照射下 HepG2 细胞 ATM 磷酸化蛋白的表注:采用集落形成法观察持续低州H亲率照射对 HepG2 细胞增殖活性的影响。结果 持续低剂量率照射 30 min 后， ATM 即已发生磷酸化，持续照射 6h 时， ATM 磷般化蛋白表达最最多，以后~渐减弱ω 使用 Wortmallnin 抑制 ATM 磷酸化后.降低了持续低剂 绩率照射下肝癌细胞的狞滔分数。结论 在持续低剂最旦在照射中后期 ATM 磷酸化减弱，提示持续 低剂量率照射具有增加 H叩G2 细胞辐射敏感性的熔能。 [关键词1 y 辐射; 肝癌细胞; 增殖; 共济失调毛细血管扩张症突变基因 ATM pho量phorylation in Heμ;2 ceUs following continuous low do悦.rate irra创ation MEl Que-lin , YANG Jian-yong ， μ Yan-hao. et al. 怜。epartment 01 Radiology. Peking University Skenzhen Hospital , Shenzhen 518036 , Chí阳 Correspondi略αuthor: llU Peng-che略• Email: liψeng _ckeng66 @ 163 . com [Abstract] Objective To investigate the change of ATM phosphoηlation ín HepG2 cells following a continuol阳 low dose- rale irr制1iation. Metb例如 Cells were persistenùy exposed 10 low dose-rate (8.28 cGy/h) irradiatíon. Indirect immunofluoresccnce and Westem blot were used 10 detect the expression of ATM phosphorylated protei阳. Colony formíng 嗣say was used to observe the effect of a low dOAe -rate irradiation on HepG2 cell survival. ResuJts After 30 min of low dose唰 rale irradiation. the phosphorylation of Aη1 occurr，时， Mter 6 h persistent írradiation , the expre幽ion of ATM phosphorylated protein reached the peak value , then gradually decre嗣ed. Aft仿r ATM phosphorylation was inhibited with Wortmannin , the surviying fraction of HepG2 cells w嗣 lower than that of the irradiation alone 陨咽up at each time point ( P 0.05). Conclusions Continuous low do!咽-rate irradiation attenuated ATM phosphorylation , suggesting that contínuous low dose-mte irra