中文摘要：

目的探讨不同水平硒摄入对实验性自身免疫性甲状腺炎（EAT）大鼠甲状腺功能、肝组织Ⅰ型脱碘酶（DⅠ）和脑组织Ⅱ型脱碘酶（DⅡ）活力的影响。方法将雌性清洁级Lewis大鼠随机分为4组：对照组、模型组、补硒＋造模组和低硒＋造模组，每组8只。适应性喂养两周后，以不同硒含量饲料干预9周，每日总硒摄入量分别为4、4、40和0．4μg，并在干预第3～8周对模型组、补硒＋造模组和低硒＋造模组大鼠进行免疫，以建立实验性自身免疫性甲状腺炎模型。观察大鼠甲状腺病理改变，测定全血硒含量、血清甲状腺自身抗体、甲状腺激素水平、DⅠ和DⅡ活力。结果模型组、补硒＋造模组和低硒＋造模组大鼠甲状腺自身抗体和甲状腺激素水平明显高于对照组（P〈0．05）。补硒＋造模组血硒含量高于对照组和模型组，而低硒＋造模组血硒含量低于对照组和模型组（P〈0．05）。此外，不同硒水平EAT大鼠甲状腺组织出现不同程度的病理损伤，缺硒组病变最严重，补硒组病变轻微。模型组DⅡ活力明显低于对照组（P〈0．05）；且与模型组相比，补硒＋造模组DⅠ和DⅡ活力升高（P〈0．05），低硒＋造模组DⅠ活力降低（P〈0．05）。结论补硒可减轻EAT所致大鼠甲状腺组织损伤，提高DⅠ和DⅡ活力；反之缺硒可加重其损伤，降低DⅠ活力。

英文摘要：

Objective To explore the effects of different levels of selenium nutrition on thyroid function, liver deiodinase type Ⅰ （D Ⅰ ） and brain deiodinase type Ⅱ （D Ⅱ ） activities in experimental autoimmune thyroiditis （EAT） rats. Methods A total of 32 female Lewis rats were randomly divided into four groups that included control group, model group, EAT with selenium- supplementation group and EAT with selenium-deficiency group. After two weeks of the basal diet administration, the rats were fed on forage containing different levels of selenium for nine weeks and the total intake of selenium were 4, 4, 40 and 0.4 μg/d, respectively. The rats of model group, EAT with selenium-supplementation group and EAT with selenium-deficiency group were induced to establish the model of experimental autoimmune thyroiditis from the third week to eighth week. The pathological change of thyroid was examined, and the levels of selenium in the blood, serum thyroid autoantibody and thyroid hormone, D Ⅰ and D Ⅱ activities were measured simultaneously. Results Compared with control group, thyroid autoantibody and thyroid hormone levels significantly increased in model group, EAT with selenium-supplementation group and EAT with selenium-deficiency group （P〈 0.05）. Compared with control and model groups, the content of selenium in the blood was increased in EAT with selenium- supplementation group, but decreased in EAT with selenium-deficiency group. Minimal pathological changes were showed in rats of EAT with selenium-supplementation group, but the pathological lesion in EAT with selenium-deficiency group was severe. D Ⅱ activity in model group was significantly decreased compared with control group. D Ⅰ and D Ⅱ activities in EAT with selenium- supplementation group were higher than those in model group （P〈0.05） and D I in EAT with selenium-deficiency group was lower than that in model group （P〈0.05）. Conclusion Selenium supplementation can relieve the damage of thyroid tissue induced by EAT a