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发育性非烯暴露触发了GPER-依赖的微质激活和随后的神经元损伤

Dianqi Yao¹, Siyu Yan², Rui Ding¹

¹Key Laboratory of Environmental Stress and Chronic Disease Control & Prevention (China Medical University), Ministry of Education, Shenyang, Liaoning, PR China.

Journal of hazardous materials

|January 14, 2026

概括

通过通过G蛋白结合雌激素受体 (GPER) 和EGFR-STAT3信号传导激活微质,导致神经元损伤和认知缺陷.

科学领域:

神经科学是一个神经科学.
环境毒理学环境毒理学
内分泌学在内分泌学.

背景情况:

诺尼尔 (NP) 是一种已知有神经毒性的环境污染物.
微质激活与NP诱导的神经元损伤有关,但潜在的机制尚不清楚.

研究的目的:

研究G蛋白结合雌激素受体 (GPER) 和其下游信号在NP诱导的微质激活和随后的神经元损伤中的作用.
阐明开发性NP暴露影响学习,记忆和神经元完整性的机制.

主要方法:

建立了一个在发育过程中暴露于环境相关的NP度的老鼠模型.
使用了NP暴露的HMC3微质和SH-SY5Y神经元的体外共同培养系统.
进行了omics分析以确定NP目标和下游信号通路,包括GPER和EGFR-STAT3.

主要成果:

发育性NP暴露导致学习/记忆缺陷,海马神经元损伤和微质激活 (M1极化,促炎细胞因子).
在海马体和体外,NP暴露激活了GPER和下游EGFR-STAT3信号.
GPER knockdown (KD) 减少了NP诱导的微质激活和神经元损伤,这种效应被STAT3激活抵消.

结论:

暴露于NP会通过以微质为中心的炎症反应触发神经元损伤.
微质GPER和下游EGFR-STAT3信号传递是NP神经毒性作用的关键媒介.
向微质GPER-EGFR-STAT3信号可能提供针对NP诱导的神经毒性的治疗策略.

关键词:

与G蛋白结合的雌激素受体受体炎症性细胞因子微质细胞中的微质细胞神经元损伤的发生.这是一种非尼尔烯.

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