高碘诱导甲状腺细胞凋亡及其机制研究  

Induction of apoptosis in thyroid cells by iodide excess and its mechanism

作　　者：刘东方[1] 邓华聪[1] 雄波 侯平 许改平[3] 

机构地区：[1]重庆医科大学临床学院内分泌科,重庆400016 [2]重庆壁山县人民医院,重庆402760 [3]重庆医科大学第二临床学院内分泌科,重庆400010

出　　处：《重庆医科大学学报》2004年第4期425-428,共4页Journal of Chongqing Medical University

基　　金：重庆市卫生局 ( 2 0 0 1-1-15 )

摘　　要：目的 :探讨高碘对正常甲状腺细胞凋亡作用及其相关机制。方法 :用不同浓度的碘化钠 (NaI)在加或不加白细胞介素 β1(IL - 1β)和甲巯咪唑 (MMI)的情况下干预培养的人正常甲状腺细胞 ,观察细胞形态的变化 ,用流式细胞仪检测细胞的凋亡率 ,免疫组化分析凋亡相关蛋白Fas、FasL、p5 3的表达情况。 结果 :用高浓度碘干预的甲状腺细胞变圆、脱壁、逐渐死亡 ,流式细胞仪检测显示甲状腺细胞随碘的剂量增加凋亡率增加 ,IL - 1β进一步促进了高碘导致的凋亡 ,而MMI可阻断高碘导致的甲状腺细胞凋亡 ,高碘处理后凋亡蛋白Fas、FasL表达明显增加 ,而p5 3却没有明显变化。结论 :高碘呈剂量依赖式的诱导甲状腺细胞的凋亡 ,IL - 1β可促进高碘的这种作用。高碘导致的甲状腺细胞凋亡主要通过Fas/FasL途径 ,而非 p5 3介导。高碘的甲状腺细胞凋亡作用并不是由碘离子 (I-)引起 ,而是与活跃的碘分子 (I2 )Objective:To explore the role of excessive iodide in inducing apoptosis in thyroid cells and its mechanism.Methods:Normal primary thyroid cells were cultured in NaI of different concentrations with or without IL-1β and methimazole.The morphological changes in thyroid cells were observed by light microscopy and apotosis rate was determined by flow cytometry techique.In the meantime Fas,FasL,p53 level were determined by histochemistry.Results:Thyroid cells treated with iodide excess underwent the morphological changes and apoptosis. There was a gradually increased apotosis rate and Fas/FasL protein expression accompanying increase in iodide concentrations.No changes in p53 protein expression was shown. IL-1β enhanced the effect of iodide cytotoxicity,whereas methimazole inhibited the role of iodide inducing apotosis.Conclusion:These data indicate that excess molecular iodide induces apoptosis in thyroid cell through Fas/FasL channel, but independent of p53.

关 键 词：高碘 甲状腺细胞 凋亡 凋亡机制 

分 类 号：R581.4[医药卫生—内分泌]