在MASLD/MASH病原体中对DDT/DDE的机制性调查:综合网络毒理学和转录学方法
Yicheng Jiang1, Yuancheng Shao1, Jiaming Xue1
1Department of Gastrointestinal Surgery, Affiliated Changzhou No.2 People's Hospital of Nanjing Medical University, The Third Affiliated Hospital of Nanjing Medical University, Changzhou Medical Center, Nanjing Medical University, Changzhou 213000, PR China.
Ecotoxicology and environmental safety
|November 13, 2025
概括
像DDT和DDE这样的环境污染物有助于与代谢功能障碍相关的脂肪性肝病 (MASLD) 和脂肪性肝炎 (MASH). 这项研究揭示了它们的毒性机制,影响着炎症和新陈代谢.
科学领域:
- 环境毒理学环境毒理学
- 肝病学 肝病学是一种肝病学.
- 分子生物学分子生物学
背景情况:
- 代谢功能障碍相关的稳态性肝病 (MASLD) 和代谢功能障碍相关的稳态性肝炎 (MASH) 是越来越多的公共卫生问题.
- 环境污染物在MASLD/MASH病原体中的具体作用尚不清楚.
研究的目的:
- 研究DDT及其代谢物DDE的肝毒性机制.
- 阐明将污染物暴露与肝病进展联系起来的分子途径.
主要方法:
- 多平台毒理学分析,包括网络毒理学和蛋白质与蛋白质相互作用 (PPI) 分析.
- 分子对接以评估DDT的结合亲和力.
- 转录基因分析,KEGG通路分析,西部抹杀,线粒体超氧化物测定和ELISA来确认发现.
主要成果:
- 暴露于DDT/DDE与IL-6,ALB,AKT1,TNF和TP53等中心介导体有关.
- 分子对接证实了DDT的高亲和度结合.
- 转录和实验数据显示了炎症和代谢途径的显著失调,氧化应激和蛋白质干扰.
结论:
- 暴露于DDT和DDE会触发一种机械路径,导致转录和蛋白质水平的变化,氧化应激和炎症.
- 这些效应是MASLD/MASH.进展的关键标志.
- 这些发现为了解污染物驱动的肝病和开发干预措施提供了基础.
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