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乙三酸通过调节IDH2/NF-κB通路和脂质过氧化,诱导肠道毒性

Kai Kang¹, Ying Huang¹

¹Department of Ultrasound, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, China.

|November 29, 2025

概括

乙支柱酸盐 (ATBC) 通过破坏IDH2/NF-κB通路引起肠损伤,导致氧化应激增加和脂质过氧化. 这项研究阐明了开发保护策略的机制,以防止塑化剂诱导的肠道毒性.

科学领域:

环境健康环境健康
毒理学毒理学毒理学
分子生物学分子生物学

背景情况:

环境污染物,包括像乙三酸 (ATBC) 这样的增塑剂,越来越多地与肠道疾病有关.
由于ATBC诱导的肠道毒性的精确分子机制在很大程度上是未知的,因此需要进一步调查.

研究的目的:

阐明由乙支酸 (ATBC) 诱导的肠道毒性的分子机制.
确定关键的分子标和涉及ATBC相关肠道损伤的途径.

主要方法:

系统地对数据库进行选 (ChEMBL,STITCH,GSE16879) 以确定ATBC目标.
使用STRING和Cytoscape识别枢纽基因的生物信息分析,然后对核心目标进行机器学习 (ATM,FYN,IDH2,TOP1).
分子对接,体外细胞实验 (NCM460,HCT116),ROS测定和JC-1染色以验证发现.

主要成果:

确定了15个枢纽基因和4个核心目标 (ATM,FYN,IDH2,TOP1),主要与NF-κB通路有关.
ATBC治疗减少了IDH2的表达,激活了NF-κB通路,增加了活性氧物种 (ROS),并导致线粒体功能障碍.
暴露于ATBC导致肠道细胞中显著的脂质过氧化和线粒体膜潜在脱极化.

结论:

通过调节IDH2/NF-κB通路并促进脂质过氧化,ATBC诱导肠道损伤.
该研究提供了对ATBC毒性的机制性理解,这对于开发预防和治疗策略对抗塑化剂诱导的肠损伤至关重要.

关键词:

ATBC ATBC 的时间在IDH2中,它是IDH2.肠道毒性肠道毒性分子对接是分子对接.网络毒理学网络毒理学

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