三酸通过cGAS-STING信号通路介导的炎症破坏肝脏脂质代谢
Liwei Yang1, Zhili Ge1, Xuehan Ding1
1Department of Occupational and Environmental Health, School of Public Health, Jilin University, Changchun 130021, China.
Toxicology letters
|January 30, 2026
概括
三聚酸 (TBP) 通过激活cGAS-STING炎症通路,导致肝损伤和脂质代谢异常. 抑制这种途径可以减少炎症,并逆转TBP诱导的肝细胞中的脂质积累.
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
- 分子生物学分子生物学
背景情况:
- 已知三酸 (TBP) 破坏肝脏脂质代谢.
- 这种cGAS-STING信号通路与炎症相关的疾病有关.
研究的目的:
- 调查TBP诱导肝脏脂质代谢障碍的机制.
- 探索cGAS-STING通路在TBP诱导的肝毒性中的作用.
主要方法:
- 使用大鼠和BRL-3A细胞模型来评估TBP肝脏毒性.
- 采用HE染色,传输电子显微镜,ELISA,Q-PCR和西部斑点来分析细胞系病理学,线粒体结构,脂质水平和基因/蛋白质表达.
- 研究了阿司匹林,RU.521和H151对TBP诱导的炎症和脂质积累的影响.
主要成果:
- 暴露于TBP会导致肝细胞胀,肝脏结构混乱以及大鼠的线粒体变化.
- TBP增加了甘油三和总胆固醇水平,以及FASN,SREBP2和PPARγ的表达.
- TBP增加了互白素-6 (IL-6) 的产生,阿司匹林可以逆转这种情况,并通过抑制细胞中的cGAS-STING通路.
结论:
- 结核血诱导显著的组织病理性肝损伤,并破坏脂质代谢.
- 该cGAS-STING信号通路调解TBP诱导的炎症反应,导致肝脏脂质的积累.
- 准cGAS-STING通路可能为TBP诱导的肝损伤提供治疗潜力.
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