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在骨髓细胞表达的触发受体 2 缺陷加剧甲基胺诱导的微细胞和神经炎症的激活

Yanxia Peng¹, Genmeng Yang¹, Shangwen Wang¹

¹School of Forensic Medicine, NHC Key Laboratory of Drug Addiction Medicine, Kunming Medical University, Kunming, China.

International journal of toxicology

|November 25, 2023

概括

甲基胺 (METH) 的使用提升了肌肉细胞2 (TREM2) 上表达的触发受体,这是微质激活和神经炎症的关键分子. TREM2 缺乏会加剧 METH 诱导的神经毒性,这表明 TREM2 是一种潜在的治疗点.

科学领域:

神经科学是一个神经科学.
免疫学免疫学免疫学
药理学药理学是指药理学的学科.

背景情况:

滥用甲基胺 (METH) 会导致神经毒性和成.
由微质细胞驱动的神经炎症与METH诱导的神经毒性有关.
在METH神经炎症中,Triggering Receptor Expressed on Myeloid Cells 2 (TREM2) 的作用尚不清楚.

研究的目的:

研究TREM2在METH诱导的神经炎症中的作用.
在METH使用者和小鼠模型中分析TREM2,TLR4,IBA1和IL-1β水平.
评估TREM2缺乏对METH诱导的神经炎症和兴奋毒性的影响.

主要方法:

对暴露于METH的野生型BV2细胞,CX3CR1^GFP/+和TREM2淘汰赛小鼠的分析.
评估TREM2,TLR4,IBA1,IL-1β,iNOS和Arg-1表达的情况.
对人类METH使用者的死后额叶皮层样本的检查.

主要成果:

在人类METH使用者和BV2细胞中,TREM2,TLR4,IBA1和IL-1β被上调.
在小鼠模型中,METH诱导了微质激活,并增加了IBA1,TREM2,TLR4和IL-1β.
在TREM2淘汰赛中,小鼠表现出严重的METH诱导的微质激活,神经炎症和兴奋毒性.

结论:

TREM2表达因METH暴露而增加.
TREM2对METH诱导的神经炎症和兴奋毒性起着保护作用.
准TREM2可能是缓解METH诱导的神经炎症的策略.

关键词:

甲基胺的使用方法神经炎症是一种神经炎症.神经毒性的作用.触发受体表达在骨髓细胞2上

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