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母体边缘性碘缺乏通过NF-κB信号通路和微管相关蛋白1B限制大鼠子代小脑浦肯野细胞的树突生长。

Maternal marginal iodine deficiency limits dendritic growth of cerebellar purkinje cells in rat offspring by NF-κB signaling and MAP1B.

作者信息

Yu Ye, Dong Jing, Wang Yuan, Wang Yi, Min Hui, Shan Zhongyan, Teng Weiping, Chen Jie

机构信息

Department of Occupational and Environmental Health School of Public Health, China Medical University, Shenyang, People's Republic of China.

Department of Endocrinology and Metabolism, Liaoning Provincial Key Laboratory of Endocrine Diseases, the First Hospital of China Medical University, Shenyang, People's Republic of China.

出版信息

Environ Toxicol. 2017 Apr;32(4):1241-1251. doi: 10.1002/tox.22320. Epub 2016 Jul 22.

DOI:10.1002/tox.22320
PMID:27444543
Abstract

Iodine deficiency (ID) during early pregnancy had an adverse effect on children's psychomotor and motor function. It is worth noting that maternal marginal ID tends to be a common public health problem. Whether marginal ID potentially had adverse effects on the development of cerebellum and the underlying mechanisms remain unclear. Therefore, our aim was to study the effects of marginal ID on the dendritic growth in filial cerebellar Purkinje cells (PCs) and the underlying mechanism. In the present study, we established Wistar rat models by feeding dam rats with a diet deficient in iodine and deionized water supplemented with potassium iodide. We examined the total dendritic length using immunofluorescence, and Western blot analysis was conducted to investigate the activity of nuclear factor-κB (NF-κB) signaling and microtubule-associated protein 1B (MAP1B). Our results showed that marginal ID reduced the total dendritic length of cerebellar PCs, slightly down-regulated the activity of NF-κB signaling and decreased MAP1B in cerebellar PCs on postnatal day (PN) 7, PN14, and PN21. Our study may support the hypothesis that decreased T induced by marginal ID limits PCs dendritic growth, which may involve in the disturbance of NF-κB signaling and MAP1B on the cerebellum. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 1241-1251, 2017.

摘要

妊娠早期碘缺乏(ID)会对儿童的心理运动和运动功能产生不利影响。值得注意的是,母体边缘性碘缺乏往往是一个常见的公共卫生问题。边缘性碘缺乏是否会对小脑发育产生潜在不利影响及其潜在机制仍不清楚。因此,我们的目的是研究边缘性碘缺乏对子代小脑浦肯野细胞(PCs)树突生长的影响及其潜在机制。在本研究中,我们通过给孕鼠喂食缺碘饮食并补充碘化钾的去离子水建立了Wistar大鼠模型。我们使用免疫荧光检查了总树突长度,并进行了蛋白质印迹分析以研究核因子-κB(NF-κB)信号通路和微管相关蛋白1B(MAP1B)的活性。我们的结果表明,边缘性碘缺乏在出生后第7天、第14天和第21天减少了小脑PCs的总树突长度,轻微下调了NF-κB信号通路的活性,并降低了小脑PCs中的MAP1B。我们的研究可能支持以下假设,即边缘性碘缺乏诱导的甲状腺素减少限制了PCs树突的生长,这可能涉及小脑NF-κB信号通路和MAP1B的紊乱。©2016威利期刊公司。《环境毒理学》32:1241 - 1251,2017。

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