摘要
目的探讨碘过量对实验性自身免疫性甲状腺炎（EAT）大鼠骨代谢的影响。方法雌性Lewis大鼠36只，体质量为（131±15）g，按体质量随机分为3组：对照组、EAT组和EAT＋高碘组，每组12只。以不同含碘量（0．9、0．9、18．0mg／kg）的饲料喂养各组大鼠，并用猪甲状腺球蛋白（pTG）和完全弗氏佐剂（CFA）对EAT组和EAT＋高碘组大鼠进行免疫以建立EAT模型。2周后观察大鼠甲状腺病理改变，测定血清甲状腺自身抗体[甲状腺球蛋白抗体（TGAb）、甲状腺微粒体抗体（TMAb）]和甲状腺激素[三碘甲腺原氨酸（T]）、甲状腺素（T4）]以及骨代谢相关指标[骨钙素（BGP）、抗酒石酸盐酸性磷酸酶（TRAP）、I型前胶原羧基末端前肽（PICP）、I型胶原羧基吡啶并啉交联肽（ICTP）、胰岛素样生长因子-1（IGF-1）、护骨素（OPG）、核因子KB受体活化因子配体（RANKL）]水平。结果EAT组和EAT＋高碘组大鼠甲状腺组织均呈现炎细胞浸润，局部滤泡结构破坏，其中EAT＋高碘组以甲状腺滤泡扩张、融合为主。EAT组和EAT＋高碘组大鼠血清TGAb、TMAb、T3和T4水平[（63．01±12．36）％、（60．62±11．24）％，（3．78±1．43）、（125．12±16．00）pmol／L和（75．00±15．44）％、（72．15±15．00）％，（3．69±0．91）、（149．40±20．67）pmol／L]高于对照组[（4．47±1．04）％、（5．73±1．01）％，（0．75±0．12）、（76．91±9．30）pmol／L，P均〈0．05]，EAT＋高碘组大鼠血清TGAb、TMAb和T4水平较EAT组升高（P均〈0．05）。EAT组大鼠血清BGP、PICP和IGF-1水平[（1．70±0．31）、（11.31±1．52）μg／L，（0．31±0．06）mg／L]较对照组[（8．60±0．33）、（14．28±3．10）μg／L，（1．16±0．02）mg／L]降低（P均〈0．05），血清TRAP、ICTP、OPG和RANKL水平[（19．88±3．60）ng／L，（2．43±0．82）、（22．36±2．80）、（1．35±0．23）μg／L]较对照组[（14．57±3．56）ng／L，（0．50±0．20）、（1．61±0．34）、（0．10±0．02）μg／L]升高（P均〈0．05）；与EAT组比较，EAT＋高碘组大鼠血清PICP和OPG水平[（8．03±1．84）、（16．80±3．79）μg／L]明显降低（P均〈0．05）。结论EAT时大鼠的破骨细胞分化与成熟增强，导致骨吸收增强。碘过量可抑制EAT大鼠成骨细胞和破骨细胞活性，呈现低转化型骨质疏松。
Objective To explore the effect of iodine excess on bone metabolism in experimental autoimmune thyroiditis（EAT） rats. Methods We selected 36 female Lewis rats with body weight of （131 ± 15）g, and divided them into 3 groups randomly： control group, EAT group and EAT ＋ high iodine group, assuring 12 rats in every group. These rats were fed fodder with different concentration of iodine（0.9,0.9,18.0 mg/kg）, and rats in EAT group and EAT ＋ high iodine group were immunized with pig thyroglobulin（pTG） and complete Freund＇s adjuvant（CFA） to create EAT model. After two weeks, the pathological changes of the thyroid tissues were observed, and the serum thyroid autoantibody [ thyroglobulin antibody （TGAb） and thyroid microsomal antibody （TMAb）], the thyroid hormone levels [triiodo thyronine（T3） and thyrine （T4）] and some relevant data of bone metabolism[bone gla protein （BGP）, tartrate-resistant acid phosphatase （TRAP）, C-terminal propeptide of type I procollagen（PICP）, C-terminal telopeptide of type I collagen （ICTP）, insulin-like growth factor- 1 （IGF- 1 ）, osteoprotegerin （OPG） and receptor activator of NF- stB ligand （RANKL） ] were measured. Results Inflammatory cell infiltration and lOcal follicular structural damage were observed in the thyroid tissues of EAT rats in EAT group and EAT ＋ high iodine group, and the pathological changes of EAT ＋ high iodine group were mainly thyroid follicular expansion and integration. The level of serum TGAb, TMAb, T3 and T4 of EAT rats in EAT group and EAT ＋ high iodine group[ （63.01 ± 12.36）%, （60.62 ± 11.24）%, （3.78 ± 1.43）, （125.12 ± 16.00）pmol/L and （75.00 ± 15.44）%, （72.15 ± 15.00）%, （3.69 ± 0.91）, （149.40 ± 20.67）pmol/Ll were ：higher than those of the control group[（4.47 ± 1.04）%, （5.73 ± 1.01）%, （0.75 ± 0.12）, （76.91 ± 9.30）pmol/L, all P 〈 0.05], and the level of serum TGAb, TMAb and T4 of EAT rats in EAT ＋ high iodine group were higher than those of the EAT group（all P 〈 0.05）. The level of serum BGP, PICP and IGF-1 in EAT group[ （ 1.70 ±0.31 ）, （ 11.31 ± 1.52） μg/L, （0.31 ± 0.06）mg/L ] were lower than those of the control group[ （8.60± 0.33）, （14.28 ± 3.10）μg/L, （1.16± 0.02）mg/L, all/b 〈 0.05], and the level of serum TRAP, ICTP, OPG and RANKL[ （19.88 ± 3.60）ng/L, （2.43 ± 0.82）, （22.36± 2.80）, （1.35 ± 0.23）μg/L] were higher than those of the control group[ （14.57 ± 3.56）ng/L, （0.50 ± 0.20）, （1.61 ± 0.34）, （0.10 ± 0.02）μg/L, all P 〈 0.051 ; compared with EAT group, the level of PCIP and OPG in EAT ＋ high iodine group [ （8.03 ± 1.84）, （16.80 ± 3.79）μg/L] were obviously decreased（all P 〈 0.05）. Conclusions The reinforcement of differentiation and maturation of osteoblast in the EAT rats results in the increasing of bone resorption. The activity of osteoblast and osteoclast of the EAT rats are inhibited by excessive iodine, showing a low conversion-type osteoporosis.
出处
《中国地方病学杂志》
CAS
CSCD
北大核心
2011年第2期123-126,共4页
Chinese Jouranl of Endemiology
基金
国家自然科学基金（30571564、30972465）
天津医科大学校基金（2008KY13）
