结合的细菌转位和胆固醇酶通过阻塞性黄中的激活热致使肝损伤恶化
Xin Shen1, Xin Zhang2, Kaiyu Li3
1Department of Pharmacy, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100021, China.
Heliyon
|September 2, 2024
概括
阻塞性黄 (OJ) 通过炎引起肝损伤,由肠道微生物群的变化和脂多糖 (LPS) 的增加驱动. 胆汁和LPS协同激活炎症通路,导致肝脏的缩和细胞死亡.
科学领域:
- 肝病学 肝病学是一种肝病学.
- 微生物学 微生物学
- 免疫学 免疫学 免疫学
背景情况:
- 阻塞性黄 (OJ) 是一种与严重肝损伤相关的疾病.
- 导致OJ引起的肝损伤的精确机制,特别是炎症细胞死亡的作用,需要进一步阐明.
研究的目的:
- 为了研究火病在阻塞性黄引起的肝损伤中的作用.
- 探索肠道微生物群,脂多糖化物 (LPS),胆汁和OJ中的肝炎炎之间的相互作用.
- 为了确定与果汁相关的肝损伤的潜在治疗点.
主要方法:
- 在老鼠中通过胆道绑定诱导的阻塞性黄.
- 使用生化标志物和组织学评估肝损伤.
- 通过免疫光学,ELISA,西部斑点和RT-PCR来研究火灭.
- 使用16S rDNA测序对肠道微生物群的分析.
- 库普弗细胞和肝细胞与胆汁和LPS的体外共培.
主要成果:
- 汁改变了肠道微生物群的组成,增加了LPS水平.
- 橄果汁肝脏中的ATP水平升高表明了亡,激活了亡途径 (NLRP3,caspase-1,gasdermin D,IL-18).
- 在体外,胆汁暴露诱导了细胞死亡,并激活了NLRP3炎症体;结合胆汁和LPS加剧了热致死.
结论:
- 肠道微生物群失调和LPS增加有助于OJ诱导的肝损伤.
- 胆汁和LPS协同作用,促进亡和烧亡,加剧肝损伤.
- 这项研究揭示了与OJ相关的肝损伤的新机制,突出了热作为一个关键过程.
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