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目的:研究骨化三醇对自身免疫性甲状腺炎模型大鼠甲状腺功能、甲状腺过氧化物酶抗体(TPOAb)、甲状腺球蛋白抗体(TGAb)及脾脏T淋巴细胞亚群的影响。方法:20只Lewis大鼠采用高碘饮水联合猪甲状腺球蛋白皮下注射的方法建立自身免疫性甲状腺炎动物模型。造模成功后大鼠随机分为模型组和骨化三醇组。经10周灌胃后,检测各组大鼠甲状腺功能三项、甲状腺抗体,流式细胞技术检测大鼠脾脏T淋巴细胞亚群的比例。结果:(1)与正常组相比,模型组及骨化三醇组大鼠促甲状腺激素(TSH)明显降低,血清游离甲状腺素(FT4)及TPOAb、TGAb明显升高,差异均具有统计学意义(P<0.01);与模型组大鼠相比,骨化三醇组大鼠TPOAb、TGAb明显降低(P<0.01);(2)与正常组相比,模型组大鼠表现为Th1、Th17细胞比例升高(P<0.05),Th1/Th2、Th17/Treg比例升高(P<0.05),与模型组相比,骨化三醇组大鼠Th1、Th17细胞比例降低(P<0.05),Th2、Treg比例升高(P<0.05),Th1/Th2、Th17/Treg比例降低(P<0.01)。结论:骨化三醇可通过抑制Th1、Th17免疫亢进,改善Th1/Th2、Th17/Treg失调,改善自身免疫性甲状腺炎免疫反应。
Objective: To study the effects of calcitriol on thyroid function, thyroid peroxidase (TPOAb), thyroglobulin antibody (TGAb) and spleen T lymphocyte subsets in autoimmune thyroiditis model rats. Methods: Twenty Lewis rats were induced with autoimmune thyroiditis by subcutaneous injection of high iodine drinking water combined with porcine thyroglobulin. After successful modeling, rats were randomly divided into model group and calcitriol group. After 10 weeks of intragastric administration, thyroid function, thyroid antibody and flow cytometry were used to detect the proportion of T lymphocyte subsets in the spleen of rats in each group. Results: (1) Compared with the normal group, the thyroid-stimulating hormone (TSH) in the model group and the calcitriol group were significantly decreased, the levels of serum free thyroxine (FT4), TPOAb and TGAb were significantly increased, the differences were statistically significant (P <0.01). Compared with the model group, TPOAb and TGAb in the calcitriol group were significantly decreased (P <0.01); (2) Compared with the normal group, the rats in the model group showed Th1, (P <0.05), and the ratio of Th1 / Th2 and Th17 / Tregs increased (P <0.05). Compared with the model group, the proportion of Th1 and Th17 cells in calcitriol group decreased (P <0.05) ), Th2, Treg (P <0.05), Th1 / Th2, Th17 / Treg ratio decreased (P <0.01). Conclusion: Calcitriol can improve the immune response of autoimmune thyroiditis by inhibiting the Th1 and Th17 immunosuppression and improving the imbalance of Th1 / Th2 and Th17 / Treg.