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化物通过NLRP3/Caspase-1/GSDMD通路促进微质中炎症因子的分泌

Qiuyi Zhang¹, Tao Li¹, Ruili Shi^1,2

¹School of Basic Medical Sciences and Forensic Medicine, Baotou Medical College, Baotou, 014040, Inner Mongolia, China.

Environmental science and pollution research international

|February 17, 2024

概括

过度的化物暴露会通过NLRP3炎症酶途径损害微质,导致细胞损伤和炎症. 这项研究澄清了化物诱导的神经炎症和热的机制.

科学领域:

神经科学是一个神经科学.
毒理学毒理学毒理学
免疫学免疫学免疫学

背景情况:

流行性化症在中国普遍存在,过度化物暴露与神经系统疾病有关.
化物损害神经系统,特别是微质细胞的确切机制尚不清楚.
NLRP3/Caspase-1/GSDMD通路是涉及各种疾病的热的关键调解者.

研究的目的:

研究化 (NaF) 在BV2微质中诱导炎症和热的分子机制.
探索NLRP3/Caspase-1/GSDMD信号通路在NaF诱导的微质损伤中的作用.

主要方法:

在不同时间 (24,48,72小时) 的时间内,BV2微质被治疗了不同度的NaF (0.25,1,2 mmol/L).
试验包括细胞活力,形态,乳酸脱酶释放以及相关蛋白质和基因表达的分析.
用于机理性验证的是一种灭酶抑制剂 - - 迪苏尔菲拉姆.

主要成果:

在剂量取决的方式中,NaF暴露诱导了BV2细胞损伤.
NaF破坏了细胞膜的完整性,并增加了IL-1β水平.
NaF提高了NLRP3,Caspase-1和GSDMD的调节,表明激光灭路径的激活.
迪苏尔菲拉姆治疗改善了NaF诱导的细胞损伤.

结论:

NaF诱导的BV2微质细胞损伤通过涉及NLRP3,Caspase-1和GSDMD的经典火灭菌途径进行介导.
这项研究阐明了化物神经毒性背后的关键分子机制.

关键词:

化物的化物.微质细胞中的微质细胞在NLRP3/Caspase-1/GSDMD中使用.热性灭症 (Pyroptosis) 是一种

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