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苏尔福拉抑制氧化应激,并可能通过调节NRF2/NLRP3信号通路在杆菌结核病感染的巨细胞中产生抗火虫作用

Guangxin Chen^1,2, Lin Shen^1,2, Hong Hu^1,2

¹Institutes of Biomedical Sciences, Shanxi University, Taiyuan 030006, China.

|June 27, 2024

概括

硫福拉 (SFN) 通过激活NRF2通路,在感染Mycobacterium tuberculosis的巨细胞中对抗氧化应激和热. 此外,SFN通过NRF2依赖和独立的机制表现出抗火虫的作用,具有治疗潜力.

科学领域:

免疫学和微生物学
分子生物学和生物化学分子生物学和生物化学

背景情况:

结核菌菌菌 (Mtb) 感染会诱导巨细胞的氧化应激和热.
硫黄 (SFN) 是一种天然化合物,它调节细胞的氧化还原平衡和NRF2信号传递.

研究的目的:

研究SFN对MTB感染巨细胞中氧化应激和热的作用.
阐明NRF2信号通路在SFN保护机制中的作用.

主要方法:

评估氧化应激标志物 (iNOS,ROS,MDA,GSH) 和NRF2通路激活 (NRF2,HO-1,NQO-1) 在接受SFN治疗的Mtb感染巨细胞中.
评估对SFN治疗的反应中的烧亡标记物 (NLRP3,Caspase-1,GSDMD,IL-1β,IL-18,LDH).
使用野生类型和NRF2缺陷巨细胞的实验来区分SFN的机制.

主要成果:

SFN治疗抑制了Mtb诱导的iNOS,COX-2,MDA和ROS,同时增强了GSH,NRF2,HO-1和NQO-1的表达,这表明通过NRF2激活减轻了氧化应激.
SFN降低了NLRP3,Caspase-1,GSDMD,IL-1β,IL-18和LDH水平,这表明它具有抗火性作用.
即使在NRF2缺乏的巨细胞中,SFN也抑制了NLRP3炎症酶激活和烧灭标志物,这表明NRF2独立的机制.

结论:

SFN主要通过NRF2通路激活来缓解Mtb感染的巨细胞中的氧化应激.
通过NRF2-依赖和独立的通路,SFN通过准NLRP3炎症体来表现出抗火虫性质.
通过不同的分子机制,SFN证明了对Mtb诱导的细胞损伤的双重治疗潜力.

关键词:

巨细胞是什么?巨细胞是什么?氧化应激是一种氧化应激.热致灭 (pyroptosis) 是一种致的过程.硫甲是一种硫甲.

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