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Updated: May 5, 2026

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Published on: August 7, 2018

RIPK3 / MLKL介导的亡促进肝炎通过饮用水通过慢性暴露促进肝炎

Meng Zhang¹, Mingzhao Jia¹, Yinan Liu¹

¹School of Public Health, Health Science Center, Xi'an Jiaotong University, NHC Key Laboratory of Environment and Endemic Diseases, No. 76 Yanta West Road, Xi'an, 710061, Shaanxi, PR China.

Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association

|February 20, 2026

概括

长期暴露于会通过亡,一种涉及RIPK3和MLKL的细胞死亡途径引起肝损伤. 抑制MLKL显著减少了小鼠的诱导的肝损伤和炎症.

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:

从受污染的水中长期暴露于是肝损伤的重大环境风险.
引起的肝毒性背后的精确机制尚未完全理解.

研究的目的:

研究受体相互作用蛋白激酶3 (RIPK3) /混合系激酶域样蛋白 (MLKL) 介导的死在诱导的肝损伤中的作用.
评估针对MLKL的治疗潜力,以减轻的肝毒性.

主要方法:

一个长期的体内小鼠模型,在饮用水中暴露于不同度的酸 (NaAsO2) 8周.
评估肝损伤标志物 (ALT,AST,GST-α,GDH),肝细胞亡,以及与亡相关的蛋白质 (p-RIPK3,p-MLKL) 和炎症性细胞因子 (TNF-α,IL-6) 的肝脏表达.
在暴露于后,野生型 (WT) 和缺乏MLKL (Mlkl-/-) 的小鼠的肝损伤的比较.

主要成果:

暴露导致了剂量依赖的肝细胞亡和肝损伤标志物的升高.
在暴露于的WT小鼠中观察到p-RIPK3,p-MLKL,HMGB1,TNF-α和IL-6的肝脏表达增加.
在高剂量暴露后,Mlkl-/-小鼠的肝损伤显著减少,肝酶和炎症标志物水平降低,HMGB1表达减少,与WT对照相比.

结论:

通过促进肝细胞死亡和炎症,RIPK3/MLKL介导的死在诱导的肝损伤中发挥着关键作用.
抑制MLKL通过减少细胞死亡和炎症,有效地减轻小鼠中引起的肝损伤.
针对MLKL是一个潜在的治疗策略,用于管理与有关的慢性肝毒性.

关键词:

亚是一种.饮用水污染饮用水污染炎症炎症是一种炎症.肝脏损伤肝脏损伤是什么?MLKL 没有使用尸体灭 (Necroptosis) 是一种死亡的过程.

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