Jin Meihui, Zhou Zheng, Zhang Li, Chen Yao, Liu Lixiang, Shen Hongmei
Centre for Endemic Disease Control, Chinese Centre for Disease Control and Prevention, Harbin Medical University, Harbin City, Heilongjiang Province, 150081, People's Republic of China.
National Health Commission & Education Bureau of Heilongjiang Province, Key Laboratory of Etiology and Epidemiology, Harbin Medical University (23618504), Harbin, China.
Biol Trace Elem Res. 2023 Feb;201(2):776-785. doi: 10.1007/s12011-022-03187-6. Epub 2022 Mar 23.
Excess iodine can cause autoimmune thyroiditis (AIT) in women, but it is unclear whether this has any implications for neurodevelopmental mechanisms in offspring. We studied the effects of experimental autoimmune thyroiditis (EAT) rats with different amounts of iodine intake on offspring brain development via the brain-derived neurotrophic factor (BDNF)-tropomycin receptor kinase B (TrkB) signaling pathway, because BDNF plays an important role in neurodevelopment. Rats in three thyroglobulin (Tg) immunized groups with varying iodine intakes (Tg (100 µg/L iodine), Tg + High-iodine I group (Tg + HI, 20 mg/L iodine), and Tg + High-iodine II group (Tg + HII, 200 mg/L iodine)) were injected with 800 µg Tg once every 2 weeks for 3 times. Rats in the control group (NI, 100 µg/L iodine) were immunized with saline. Arsenic-cerium catalytic spectrophotometry was used to measure urine iodine levels. The lymphocytic infiltration in the thyroids was observed by histopathological studies. Thyroid autoantibodies levels were measured using radioimmunoassay. The norepinephrine (NE) contents were measured by an enzyme-linked immunosorbent assay. The levels of the BDNF-TrkB signaling pathway and related genes were measured by quantitative real-time PCR and Western blot. Urinary iodine levels increased as iodine intake increased. Lymphocytes were significantly aggravated in Tg-immunized rats. Serum thyroglobulin antibody (TgAb) and thyroid peroxidase antibody (TPOAb) levels were clearly elevated in Tg-immunized rats. Tg-immune groups had significantly lower NE levels. The BDNF-TrkB signaling pathway and related gene mRNA and protein levels were found to be significantly lower in Tg-immune groups with higher iodine levels. Maternal AIT may reduce the levels of certain neurodevelopmental mechanisms in the offspring, such as the BDNF-TrkB signaling pathway and related factors, while excessive iodine consumption by the mother may exacerbate this effect.
过量碘可导致女性自身免疫性甲状腺炎（AIT），但尚不清楚这是否会对后代的神经发育机制产生影响。我们通过脑源性神经营养因子（BDNF）-原肌球蛋白受体激酶B（TrkB）信号通路，研究了不同碘摄入量的实验性自身免疫性甲状腺炎（EAT）大鼠对后代脑发育的影响，因为BDNF在神经发育中起重要作用。将三组不同碘摄入量的甲状腺球蛋白（Tg）免疫大鼠（Tg（100μg/L碘）、Tg +高碘I组（Tg + HI，20mg/L碘）和Tg +高碘II组（Tg + HII，200mg/L碘））每2周注射一次800μg Tg，共注射3次。对照组（NI，100μg/L碘）大鼠用生理盐水免疫。采用砷铈催化分光光度法测定尿碘水平。通过组织病理学研究观察甲状腺中的淋巴细胞浸润情况。采用放射免疫法测定甲状腺自身抗体水平。采用酶联免疫吸附测定法测定去甲肾上腺素（NE）含量。通过定量实时PCR和蛋白质印迹法测定BDNF-TrkB信号通路及相关基因的水平。尿碘水平随碘摄入量增加而升高。Tg免疫大鼠的淋巴细胞浸润明显加重。Tg免疫大鼠血清甲状腺球蛋白抗体（TgAb）和甲状腺过氧化物酶抗体（TPOAb）水平明显升高。Tg免疫组的NE水平显著降低。在碘水平较高的Tg免疫组中，BDNF-TrkB信号通路及相关基因的mRNA和蛋白质水平显著降低。母体AIT可能会降低后代某些神经发育机制的水平，如BDNF-TrkB信号通路及相关因子，而母亲过量摄入碘可能会加剧这种影响。
