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目的:探究补充维生素D对桥本甲状腺炎(Hashimoto′s thyroiditis, HT)的影响及作用机制。方法:选取雌性SD大鼠应用随机数字表法随机分为对照组、实验性自身免疫性甲状腺炎(experimental autoimmune thyroiditis, EAT)空白模型组(模型组)、小剂量(VD1组)和大剂量(VD2组)活性维生素D干预组。比较各组间甲状腺细胞形态、甲状腺功能、甲状腺抗体、各类CD4 ＋T细胞及相关细胞因子水平。 结果:模型组甲状腺过氧化物酶抗体(thyroid peroxidase antibody, TPOAb)和甲状腺球蛋白抗体(thyroglobulin antibody, TgAb)水平较对照组显著升高，VD1组和VD2组较模型组明显下降( P<0.05)。相比对照组，模型组HE染色示甲状腺组织内大量滤泡上皮细胞破坏，滤泡体积明显变小；相比模型组，VD1组和VD2组滤泡上皮细胞萎缩及破坏程度减轻。模型组辅助性T细胞(helper T cell, Th)1和Th17细胞比例及相关细胞因子水平显著高于对照组，而VD1组和VD2组均低于模型组( P<0.05)；模型组调节性T细胞(regulatory T cell, Treg)比例及相关细胞因子水平显著低于对照组，而VD1组和VD2组均高于模型组( P<0.05)。 结论:补充维生素D后，EAT大鼠的TPOAb和TgAb水平下降，各类CD4 ＋T细胞数量及相关细胞因子水平均趋于正常，提示维生素D可能通过调节CD4 ＋T细胞的分化改善HT，从而为补充维生素D在治疗HT中的作用提供理论依据。

Objective:To investigate the effect and mechanism of vitamin D supplementation on Hashimoto′s thyroiditis(HT).Methods:Female SD rats were randomly divided into four groups by random number table method: control group, experimental autoimmune thyroiditis(EAT) control model group(model group), low-dose(VD1 group) and high-dose(VD2 group) active vitamin D intervention groups. The morphology of thyroid cells, thyroid function, thyroid antibodies, various CD4 + T cells, and related cytokine levels among different groups were compared. Results:The levels of thyroid peroxidase antibody(TPOAb) and thyroid globulin antibody(TgAb) in model group were significantly higher than those in control group, while the levels of VD1 and VD2 groups were significantly lower than those in model group( P<0.05). Compared with control group, HE staining in model group showed severe damage of follicular epithelial cells; Compared with model group, the degree of atrophy and destruction of follicular epithelial cells in VD1 and VD2 groups were reduced. The proportion of helper T cell(Th)1 and Th17 cells and related cytokine levels in model group were significantly higher than those in control group, while those in VD1 and VD2 groups were lower than those in model group( P<0.05); The proportion of regulatory T cell(Treg) cells and related cytokine levels in model group were significantly lower than those in control group, while those in VD1 and VD2 groups were higher than those in model group( P<0.05). Conclusions:After supplementing with vitamin D, the levels of TPOAb and TgAb in EAT rats decreased, and the number of various CD4 + T cells and related cytokine levels tended towards normalization. This suggests that vitamin D may improve HT by regulating CD4 + T cell differentiation, providing a theoretical basis for the role of vitamin D supplementation in HT treatment.