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通过促进铁亡,NNMT参与了脱氧尼瓦诺诱导的肝细胞毒性

Weiling Huang¹, Chenchen Song², Yu Hua³

¹Department of Pediatrics, Xianning Central Hospital, The First Affiliated Hospital of Hubei University of Science and Technology, Xianning 437100, China.

|February 21, 2025

概括

脱氧尼瓦伦醇 (DON) 毒素通过促进细胞死亡途径铁亡,导致肝损伤. 这项研究表明,DON诱导的尼古丁胺N-甲基转移酶 (NNMT) 通过抑制关键蛋白质而加剧这种损伤.

科学领域:

肝病学肝病学是一种肝病学.
毒理学毒理学毒理学
细胞生物学细胞生物学

背景情况:

脱氧尼瓦伦醇 (DON) 是一种普遍存在的真菌毒素,引起显著的肝毒性.
铁亡与DON诱导的肝损伤有关,但潜在的机制尚不清楚.
尼古丁胺N-甲基转移酶 (NNMT) 表达是由DON上调调节的,但其在DON肝毒性中的作用尚不清楚.

研究的目的:

研究DON在肝细胞中诱导铁亡的机制.
阐明尼古丁胺N-甲基转移酶 (NNMT) 在DON诱导的肝毒性和铁死中的作用.

主要方法:

利用HepG2细胞研究DON诱导的铁亡.
操纵了NNMT表达 (过度表达和沉默/抑制) 以评估其对铁亡标记物的影响.
使用SLC7A11和GPX4的抑制剂来确认该途径.

主要成果:

DON暴露抑制了SLC7A11/GPX4,增加了细胞质自由Fe2+和脂质ROS,诱导了HepG2细胞中的铁亡.
过度表达NNMT通过降低SLC7A11,GPX4,GCLC和NQO1的调节,并增加Fe2+和脂质ROS,加剧了DON诱导的铁亡.
沉默/抑制NNMT扭转了这些效应,并消除了DON诱导的铁亡.

结论:

DON诱导的NNMT通过抑制SLC7A11/GPX4通路,促进HepG2细胞中的铁亡.
这些发现为控制DON肝毒性和肝细胞癌的发展提供了洞察力.

关键词:

脱氧尼瓦伦 (deoxynivalenol) 是一种除氧化.铁化是铁化的一种.肝细胞毒性肝细胞毒性尼古丁胺N-甲基转移酶的使用

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