碘通过影响细胞自噬参与甲状腺炎发病机制的研究  

Iodine regulates the pathogenesis of thyroiditis by affecting autophagy

作　　者：毕文 聂春磊[1] 张杰武[1] Bi Wen;Nie Chunlei;Zhang Jiewu(Department of head and neck surgery,Harbin medical university cancer hospital,Harbin 150031,China)

机构地区：[1]哈尔滨医科大学附属肿瘤医院、头颈外科甲状腺病区,150031

出　　处：《国际免疫学杂志》2018年第6期599-603,共5页International Journal of Immunology

基　　金：哈尔滨医科大学附属肿瘤医院海燕科研基金(JJZD2017-03)。

摘　　要：目的 探究过量碘对甲状腺细胞自噬的影响以及其与甲状腺炎发病机制的关系.方法体内实验:实验小鼠20只,随机分为实验组和对照组,每组均为10只,实验组构建小鼠甲状腺炎模型,分别检测两组小鼠血清甲状腺球蛋白抗体(thyroglobulin antibody,TGAb),甲状腺过氧化酶抗体(thyroid peroxidase antibody,TPOAb)含量;对两组小鼠的甲状腺组织进行苏木精-伊红(hematoxylin eosin,HE)染色,并用免疫组织化学法检测甲状腺组织中与自噬有关的蛋白[哺乳动物雷帕霉素靶蛋白(mammalian target of rapamycin,mTOR)、微管相关蛋白1轻链3(microtubule-associated protein1lightchain3,MAP-LC3)]以及凋亡相关蛋白半胱氨酸天冬氨酸蛋白酶-3(caspase-3)表达水平;蛋白质印迹(Western blotting,WB)法检测甲状腺组织m TOR、LC3表达.体外试验:收集正常小鼠的甲状腺组织进行细胞培养,以不同浓度的碘化钾(kalium iodine,KI)处理甲状腺细胞,利用WB法检测甲状腺细胞中m TOR、LC3表达.结果 体内实验:实验组小鼠血清中TGAb和TPOAb水平均高于对照组,差异具有统计学意义(P<0.05);实验组小鼠腺泡部分发生扩张,腺泡腔内胶质稀薄,上皮细胞肿胀破坏,淋巴细胞浸润及嗜酸性粒细胞可见;甲状腺炎小鼠的甲状腺组织中与自噬有关的蛋白mTOR蛋白高表达、LC3B-Ⅱ蛋白低表达,自噬水平低下;caspase-3表达增加,凋亡增加.同时体外实验显示,碘化钾处理使甲状腺细胞m TOR表达水平明显升高,而LC3B-Ⅱ表达水平明显下降,以10 mmol/L碘化钾处理时变化最为明显.结论 碘可能通过影响细胞自噬水平来影响甲状腺炎的发病.Objective To explore excess iodine on the autophagy of thyroid cells and the relationship with the pathogenesis of thyroiditis. Methods In vivo,20 mice were randomly divided into the experimental group and the control group,10 in each group. The mouse thyroiditis model was constructed in experimental group. Serum thyroglobulin antibody(TGAb)and thyroid peroxidase antibody(TPOAb)were detected and Hema-toxylin eosin(HE)staining was performed on thyroid tissue. The expression of autophagy related protein [mam-malian target of Rapamycin(m TOR),microtu-blule-associated protein1lightchain 3(MAP-LC3)]and caspase-3 in thyroid tissue of mice with thyroiditis was detected by immunohistochemistry and compared with normal thy-roid tissue. The expression of autophagy related proteins in thyroid tissue was detected by Western blot(WB). In vitro,cells from thyroid tissue of normal mice were cultured,and the thyroid cells were treated with different con-centrations of kalium iodine(KI),and the changes of autophagy related proteins were detected by WB. Results In vivo experiments,the levels of TGAb and TPOAb in the experimental group were higher than those in the control group,and the difference was statistically significant(P < 0. 05);in the experimental group,the acinar partialdy expanded,the colloid in the acinar cavity was thin,the epithelial cells were swollen and destroyed,the lymphocyte infiltration and eosinophils were visible;it showed that the high expression of protein mTOR expand-ed and caspase-3,low expression of LC3B- Ⅱ protein,low autophagy and high apoptosis in the thyroid tissue of the infected mice. At the same time,in vitro experiments,it showed that the expression of mTOR in thyroid cells increased significantly,while the expression level of LC3B-Ⅱ decreased significantly,and the change of 10 mmol/ L iodide treatment was the most obvious. Conclusion Iodine may affect the pathogenesis of thyroiditis by affecting the level of autophagy.

关 键 词：碘 细胞自噬 甲状腺炎 

分 类 号：R581.4[医药卫生—内分泌]