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亚斯巴甜通过线粒体功能障碍和ERK/CREB1通路抑制加剧脑缺血-再损伤

Yan Bai¹, Ji Feng¹, Xiao-Yu Wu¹

¹School of Public Health, Fudan University, Shanghai 200032, China.

Ecotoxicology and environmental safety

|February 28, 2026

概括

阿斯巴甜通过破坏线粒体和抑制ERK/CREB1通路,使中风后的大脑损伤恶化. 这种非营养甜味剂增加了细胞死亡和炎症,突出了潜在的风险.

科学领域:

神经科学是一个神经科学.
毒理学毒理学毒理学
生物化学生物化学

背景情况:

阿斯巴甜是一种常见的非营养甜味剂,可疑具有神经毒性.
大脑缺血-再输损伤 (CIRI) 是中风预后的一个重要因素.
阿斯巴甜对CIRI的影响及其机制尚不清楚.

研究的目的:

调查阿斯巴甜的消费是否会加剧CIRI.
阐明阿斯巴甜对CIRI的影响的潜在分子机制.

主要方法:

给小鼠服用阿斯巴甜,并进行诱导的CIRI.
在体外研究中使用了海马神经干细胞 (NSCs),暴露在氧气-葡萄糖剥夺 (OGD) 和阿斯巴甜中.
评估了细胞损伤,活性氧物种 (ROS),线粒体功能和ERK/CREB1通路.

主要成果:

阿斯巴甜在小鼠中增加了心脏病发作量和神经元损伤.
在NSC中,阿斯巴甜增强了OGD诱导的亡,线粒体功能障碍和ROS积累.
阿斯巴甜抑制了ERK/CREB1酸化,增加了促炎性细胞因子,并减少了神经元标记物,ERK激活部分扭转了效应.

结论:

亚斯巴甜通过压力依赖的线粒体功能障碍,ROS积累和ERK/CREB1抑制加剧了CIRI.
需要进一步的研究来探索长期的神经行为效应和临床相关性.

关键词:

亚斯巴甜胺是一种大脑缺血再输血损伤通过ERK/CREB1路径.线粒体功能障碍线粒体功能障碍线粒体的反应性氧物种.

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