乙二烯调节肝细胞模型中的炎症和细胞纤维化信号
Suryakant Niture1,2, Sashi Gadi1, Hieu Hoang1
1The Julius L. Chambers Biomedical/Biotechnology Research Institute (JLC-BBRI), North Carolina Central University (NCCU), Durham, NC 27707, USA.
Toxics
|January 8, 2025
概括
来自原油暴露的乙醇 (ETs) 影响肝细胞,增加氧化应激和炎症. 虽然不引起肥胖症,但ET改变细胞代谢和纤维化标志物,可能破坏肝功能.
科学领域:
- 毒理学 毒理学 毒理学
- 肝病学 肝病学是一种肝病学.
- 环境健康 环境健康
背景情况:
- 原油油分C9基,特别是乙烯 (ETs),是环境污染物.
- 职业和环境接触ET可以通过吸入和摄入发生.
- 之前的研究表明,外星人准呼吸道和肝脏,造成病变.
研究的目的:
- 研究低度ET异构体 (2-ET,3-ET,4-ET) 对肝细胞模型的影响.
- 评估对细胞代谢,炎症,肥胖症和纤维化信号传递的影响.
- 使用HepaRG,HepG2和SK-Hep1细胞系进行体外分析.
主要方法:
- 肝细胞模型对单个ET异构体的剂量依赖性暴露.
- 实时监测细胞生存和增殖的情况.
- 测量反应性氧物种 (ROS) 生产.
- 分析炎症,代谢,脂质发生和纤维化基因表达.
- 评估线粒体呼吸和细胞能量.
主要成果:
- ET暴露增加了ROS的产生和调节的炎症基因表达 (CAT,SOD1,CXCL8,IL1B,HMOX1,NAT1,STAT3).
- 细胞能量和代谢基因表达 (CYP1A1,CYP1A2,CYP2D6,CYP2E1,CYP3A4,CYP3B4,VEGFA) 的调高.
- 没有观察到与脂质生成相关的基因表达或细胞稳定症的显著变化.
- ET暴露调节纤维化标志物 (AST,FGF-23,Cyt-7 p21,TGFβ,TIMP2,MMP2),特别是在慢性2-ET暴露的情况下.
结论:
- 乙烯对肝细胞代谢,炎症和纤维化信号产生影响.
- 外星人会增加氧化应激,并改变肝细胞中的线粒体呼吸.
- 虽然ETs不会诱导肥胖症,但它们可能通过向纤维化途径来调节肝功能.
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