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目的观察化学缺氧剂二氯化钴(CoCl_2)诱导缺氧条件下,Eca109食管癌细胞的细胞周期及凋亡变化,并观察缺氧对放射敏感性的影响。方法CoCl_2用于建立Eca109食管癌细胞体外缺氧培养模型,并设对照组(CoCl_2浓度为0μmol)。流式细胞仪(FCM)检测缺氧培养不同时相(0、8、16、24h)Eca109细胞株细胞周期和凋亡的变化;集落形成实验观察细胞的放射敏感性。结果CoCl_2诱导Eca109细胞缺氧0—24h,随着缺氧时间的延长,处于G0/G1期的细胞明显增加,S期细胞减少。而G2/ M期、凋亡无影响(P>0.05);~(60)Coγ射线5Gy照射,缺氧加照射组G0/G1期细胞增加、G2/M期细胞减少。单纯照射组G0/G1期细胞减少,G2/M期细胞增加。克隆形成实验结果显示,缺氧组和对照组的Eca-109细胞的D0值分别为2.44Gy和2.48Gy,存活分数分别为97.33%和96.33%;缺氧组和对照组Eca-109细胞的Dq值分别为2.89Gy和0.52Gy,照射4Gy后,细胞存活分数分别为48.3%和21.7%,缺氧条件下Eca109细胞放射敏感性降低。结论CoCl_2诱导缺氧影响Eca109细胞的细胞周期,并使细胞放射敏感性降低。
Objective To observe the changes of cell cycle and apoptosis in Eca109 esophageal cancer cells induced by cobalt chloride (CoCl2), an inhibitor of hypoxia, and observe the effect of hypoxia on radiosensitivity. Methods CoCl2 was used to establish an in vitro hypoxic culture model of Eca109 esophageal cancer cells. The control group (CoCl2 concentration was 0μmol) was established. Cell cycle and apoptosis of Eca109 cells were detected by flow cytometry (FCM) at different time points (0, 8, 16, 24 hours). Colony formation assay was used to observe the cell radiosensitivity. Results CoCl2-induced Eca109 cells hypoxia 0-24h, with hypoxia time, cells in G0 / G1 phase increased significantly, S phase cells decreased. (P <0.05). G2 + M phase cells were increased in the G0 / G1 phase of hypoxia plus irradiation, while cells in the G2 / M phase were decreased. In the simple irradiation group, the number of G0 / G1 phase cells decreased and G2 / M phase cells increased. The results of clone formation showed that the D0 values of Eca-109 cells in hypoxia group and control group were 2.44Gy and 2.48Gy, respectively, and the survival scores were 97.33% and 96.33% respectively. The Dq of Eca-109 cells in hypoxia group and control group were The values of which were 2.89Gy and 0.52Gy, respectively. After 4 days of irradiation, the cell survival scores were 48.3% and 21.7%, respectively. The radiosensitivity of Eca109 cells was reduced under hypoxia. Conclusion CoCl2-induced hypoxia affects the cell cycle of Eca109 cells and decreases the radiosensitivity of Eca109 cells.