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参与PI3K/Nrf2路径在大鼠的诱导内分泌和甲状腺毒性

Xiaowei Ma¹, Yujian Zheng¹, Hongyun Li¹

¹School of Public Health, Key Laboratory of Special Environmental and Health Research, Xinjiang Medical University, Urumqi, China.

Journal of applied toxicology : JAT

|September 10, 2025

概括

暴露会通过改变PI3K/Nrf2通路来破坏甲状腺功能和内分泌平衡. 这项研究揭示了酸如何影响甲状腺细胞和老鼠模型,影响激素水平和基因表达.

科学领域:

环境毒理学环境毒理学
内分泌学在内分泌学.
分子生物学分子生物学

背景情况:

(As) 暴露与各种疾病有关,可能通过甲状腺和内分泌系统的毒性.
引起的内分泌干扰背后的确切机制尚不清楚.
研究特定分子通路的作用对于了解对健康的影响至关重要.

研究的目的:

调查酸丁3-激酶 (PI3K) 和NF-E2相关因子2 (Nrf2) 途径对酸 (NaAsO2) 诱导的甲状腺和内分泌系统毒性的参与.
在体外甲状腺细胞模型和体外大鼠模型中阐明毒性的分子机制.

主要方法:

试验室内:甲状腺毛囊上皮细胞暴露于不同度的NaAsO2.
在体内:Wistar大鼠在20周的时间内以不同的剂量给予NaAsO2.
进行了基因表达分析 (ERα,TRα,Keap1,Nrf2,PI3K,AKT的mRNA水平) 和血清激素水平测量.

主要成果:

在体外和体内,NaAsO2暴露降低了三铁素 (T3) 和甲状腺素 (T4) 的水平.
在大鼠中观察到血清雌激素 (E2) 的增加和甲状腺激素代谢的改变.
在这两种模型中,NaAsO2暴露上调了ERα,TRα,Nrf2和PI3K的mRNA表达,同时降低了Keap1和AKT的表达.

结论:

暴露于酸酸盐会诱导细胞毒性,并破坏雌激素的产生,导致甲状腺功能障碍.
PI3K/Nrf2通路在调解对甲状腺和内分泌系统的毒性影响方面发挥着重要作用.
这些发现突出了引起的甲状腺功能和内分泌平衡的复杂机制.

关键词:

Nrf2 没有任何问题.在PI3K中,PI3K是指PI3K.亚是一种.内分泌干扰干扰内分泌系统甲状腺毒性甲状腺毒性

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