在素诱导的炎症性损伤中,自和炎症体之间的交叉交互
Shiji Zhang1, Na Zhao2, Suli Song3
1Inner Mongolia Minzu University, Inner Mongolia 028000, PR China.
Toxicology and applied pharmacology
|March 16, 2024
概括
素毒素 (RT) 导致器官损伤和炎症. 激活自,就像拉巴胺一样,可以抑制RT诱导的NLRP3炎症酶激活,为酸盐中毒提供潜在的治疗方法.
科学领域:
- 毒理学 毒理学 毒理学
- 细胞生物学 细胞生物学
- 免疫学 免疫学 免疫学
背景情况:
- 素毒素 (RT) 导致严重的多器官损伤,目前没有抗药.
- 转基因中毒包括蛋白质合成抑制,氧化应激,炎症和自.
- 了解RT的炎症机制对于开发治疗方法至关重要.
研究的目的:
- 研究RT诱导的细胞损伤中自和NLRP3炎症体之间的相互作用.
- 确定用于预防和治疗素中毒的特定分子标.
主要方法:
- 通过TLR4/MyD88/NLRP3信号传递和ROS产生特征的RT诱导炎症.
- 在RT暴露细胞中评估了自标志物 (ATG5,p62,Beclin1,LC3点).
- 评估了拉帕素 (Rapa),MCC950,MyD88敲击和NAC对RT诱导炎症的影响.
主要成果:
- RT激活了TLR4/MyD88/NLRP3信号传输,增加了ROS,并增强了自.
- ASC斑形成和IL-1β,IL-6,TNF-α表达被MCC950,MyD88淘汰和NAC降低.
- 拉巴胺治疗逆转了RT诱导的信号激活和炎症性细胞因子的产生.
结论:
- 素毒素促进NLRP3炎症酶激活和自.
- 自的激活,以拉巴胺治疗为例,通过抑制NLRP3炎症酶来减轻RT诱导的炎症.
- 拉巴胺显示出作为治疗素诱导的炎症疾病的治疗剂的潜力.
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