IL-2对中子照射后肠上皮细胞生长和凋亡的影响及其机制  

Effect of IL-2 on the growth and apoptosis of intestinal epithelial cells radiated by neutron and mechanisms of IL-2 on the injured IEC-6

作　　者：付凯飞[1] 彭瑞云[1] 高亚兵[1] 王德文[1] 罗庆良[1] 董波[1] 马俊杰[1] 

机构地区：[1]军事医学科学院放射与辐射医学研究所,北京100850

出　　处：《细胞与分子免疫学杂志》2007年第8期723-726,共4页Chinese Journal of Cellular and Molecular Immunology

基　　金：全军"十一五"医药卫生科研基金专项项目(06Z064);国家自然科学基金资助项目(30370438)

摘　　要：目的:观察中子照射对体外培养的IEC-6细胞生长的影响及IL-2对其损伤后增殖和恢复的作用,并进一步探讨IL-2调节受照射肠上皮细胞生长的相关机制。方法:单独用IL-2(1×105U/L)或同时施加JAK1激酶阻断剂(A77-1726)处理受4Gy中子照射的IEC-6细胞,并于照后10、15、30min和1、3、6、12、24、48及72h,用MTT比色法和流式细胞术检测受照射后IEC-6细胞的增殖活力和死亡方式的改变。以免疫细胞化学染色和Western blot检测IEC-6细胞上IL-2Rβ的表达和JAK1活化情况。结果:4Gy中子照射后24h,IEC-6细胞的增殖活力明显降低;而IL-2处理组该细胞的增殖活力有显著提高(P<0.05)。受中子照射的IEC-6细胞经IL-2作用24h,其凋亡率明显降低(P<0.05),而坏死率变化不明显。以IL-2刺激中子照射的IEC-6细胞后,于10及15min可见JAK1发生明显磷酸化活化,24h时IL-2Rβ的表达明显增多。同时应用A77-1726和IL-2处理受中子照射的IEC-6细胞后,其增殖活力明显低于单纯IL-2处理组。结论:IL-2可促进受中子照射的IEC-6细胞增殖,具有抗辐射作用。IL-2Rβ和JAK1活化参与了IL-2对中子损伤的IEC-6细胞生长的调控。AIM： To observe the effect of neutron radiation on intestinal epithelial cells 6 （IEC-6）, to study the effect of IL-2 on the proliferation and recovery of neutron-injured IEC-6, and to investigate the regulatory mechanisms of IL-2 on the injured IEC-6. METHODS： 4 Gy-neutron-injured IEC-6 were treated by IL-2, with or without the blocking agent JAK1 （A77-1726）. The change of proliferative activity and death manner of the treated IEC-6 were detected by MIT colorimetry and flow cytometry at 10, 15, 30 minutes and 1,3, 6, 12, 24, 48, 72 hours respectively. The expres- sion of IL-2Rβ and the activation of JAKI of neutron-injured IEC-6 treated by IL-2 were detected by immunocytochemical stainning and Western blot. RESULTS： After IEC-6 were radiated by 4 Gy neutron for 24 hours, the proliferative activity of IEC-6 decreased markedly but increased strikingly after IL-2 treatment（P〈0.05）. The apoptosis of IEC-6 in IL-2-treated group decreased （ P 〈 0.05 ）, but there was no obvious defference in necrotic cell number. After neutron-injured IEC-6 were treated by IL-2, JAK, was activated at 10 and 1.5 minutes, and the expression of IL-2Rβ increased apparently at 24 hours. When treated by JAK1 and IL-2, the proliferative activity of neutron-injured IEC-6 was much lower than that in IL-2-treated group. CONCLUSION： IL-2 can accelarate the proliferation of neutron-radiated IEC-6 and protect them from neutron injury. IL-2Rβ and JAK1 participate in the regulation of neutron-injured IEC-6 by IL-2.

关 键 词：中子辐射 IEC-6 IL-2 IL-2Rβ JAK1 

分 类 号：R392[医药卫生—免疫学] R146[医药卫生—基础医学]