中文摘要：

目的制备碘缺乏小鼠模型，检测促甲状腺激素（TSH）B剪接变体（TSHβ-v）是否受循环中甲状腺激素的调节，探讨免疫系统来源的TSHβ-V在维持甲状腺自稳态中的作用。方法选用离乳BALB／c小鼠20只，雌雄各半。小鼠按体质量和性别随机分为2组，每组10只。对照组：饮去离子水，普通饲料喂养；低碘组：饮去离子水，低碘饲料（含碘量20～40ug／kg）喂养，每日碘摄入量约为0．25ug／d。3个月后处死小鼠，化学发光免疫分析法（CIA）检测小鼠血清中甲状腺激素和TSH水平，实时定量（RT）-PCR法测定小鼠骨髓、外周血、甲状腺、垂体TSHβ-V的表达。结果低碘组小鼠血清总甲状腺素（TT4）、游离甲状腺素（FT4）、总三碘甲腺原氨酸（TT3）、游离三碘甲腺原氨酸（FT3）[（0．47±0．70）nmol／L、（2．41±0．28）pmol／L、（0．76±0．08）nmol／L、（4．01±0．40）pmol／L]显著低于对照组[（55．2±3．68）nmol／L、（32．72±1．02）pmol／L、（1．10±0．06）nmol／L、（5．40±0．38）pmol／L，t=43．81、86．04、9．81、7．51，P均〈0．01]；低碘组小鼠TSH[（35．67±17．39）mU／L]明显高于对照组[（0．24±0．10）mU／L，t=-6．11，P〈0．001]；低碘组小鼠骨髓、外周血TSHβ-VmRNA表达水平[（9．62±0．60）、（9．25±0．83）]均低于正常对照组（7．69±0．36、7．11±0．41，t=6．77、5．64，P均〈0．001）；低碘组小鼠甲状腺TSHβ-VmRNA表达（9．32±0．91）与对照组（9．12±0．62）相比较，差异无统计学意义（t=0．45，P〉0．05）；在骨髓、外周血、甲状腺未检出天然型TSHβ；垂体中TSHβ-VmRNA和天然型TSHβ表达水平（1.99±0．61、-7．17±1．78）均高于对照组（5．75±0．98、-1．43±0．51，t=-8．02、-7．60，P均〈0．01]。结论低碘饮食引发小鼠甲状腺功能低下，抑制骨髓和外周血TSHβ-VmRNA的表达，提示免疫系统来源的T

英文摘要：

Objective To find out if the immune system derived thyroid stimulating hormone（TSH） β splice variant（TSHβ-V） would be regulated by circulating thyroid hormone levels to get a further understanding of the function and mechanism of this TSHβ-V in thyroid homeostasis. Methods A total of 20 weaning Balb/c mice （half male and half female） were selected and randomly divided into two groups according to their body mass and gender（n = 10）. Mice of control group were fed with common diet and deionized water. Mice of the low-iodine（U） group were fed with low-iodine diet（containing iodine 20 - 40 ug/kg, iodine-intake about 0.25 ug,/d） and deionized water. The experimental period was 3 months. At the end of the experiment, mice were executed and the blood was collected to observe the levels of TSH and thyroid hormone by chemiluminescence immunoassay（CIA） ; bone marrow （BM）, peripheral blood（PBL）, thyroid gland and pituitary were collected to assay＇ the TSHβ-V mRNA expression by real-time quantitative reverse transcriptase polymerase chain reaction （RT-PCR）. Results The serum free thyroxine（FT4） and total thyroxine（TT4） levels in LI group of mice[（0.47 ± 0.70）nmoL/L, （2.41 ± 0.28）pmoL/L] were significantly lower than that of the control group of mice [ （55.2 ± 3.68） nmol/L, （32.72 ± 1.02） pmoL/L, t = 43.81,86.04,all P 〈 0.01 ] and the serum total triiodothyronine（TT3） and free triiodothyronine（FT3） reduction in LI group of mice [ （0.76± 0.08）nmol/L, （4.01± 0.40）pmol/L] were significantly lower than that of the control group of mice [ （1.10 ± 0.06）nmol/L, （5.40 ± 0.38）pmol/L, t = 9181,7.51, P 〈 0.01]. Iodine insufficiency strongly elevated the serum TSH in LI group of mice [ （35.67 ± 17.39 ）mU/L ] than that in control group of mice [ （0.24 ± 0.10）mU/L, t = - 6.11, P〈 0.01]. The mRNA levels ofTSH β-V in BM（9.62 ± 0.60） and in PBL（9.25 ± 0.83） of LI group of mice were lower than those in control group