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微塑料暴露会通过激活NF-κB和NRF2/KEAP1信号来加剧SLE中的协同炎和烧伤

Wenxiang Zeng^1,2, Shiqiao He^1,2, Ying Zhao^3,4

¹The Third Clinical Medical College, Zhejiang Chinese Medical University, Hangzhou 310053, China.

|January 8, 2025

概括

微塑料 (MPs) 暴露会在狼性关节炎中恶化关节炎症. 在系统性红斑狼 (SLE) 的小鼠模型中,MPs会引起突损伤,氧化应激和细胞死亡,影响膝关节关节的健康.

科学领域:

环境健康环境健康
类风湿病学类风湿病学
毒理学毒理学毒理学

背景情况:

微塑料 (MP) 是新兴的环境污染物,具有潜在的人类健康风险.
系统性红斑狼 (SLE) 是一种自身免疫性疾病,通常涉及关节炎症.
国会议员对狼性关节炎的影响仍未得到充分研究.

研究的目的:

为了研究微塑料暴露对SLE小鼠模型关节炎的影响.
阐明MP可能加剧狼性关节炎的机制.

主要方法:

用MPs (0.5 mg/kg或5 mg/kg) 口服给8周大的雌性MRL/lpr小鼠,这是人类SLE的一个模型.
评估膝关节形态,功能,氧化应激,亡,纤维化和炎症性细胞因子分泌.
分析与热致死相关的基因表达 (NLRP3,CASPASE-1,GSDMD,IL-1β,IL-18) 和信号通路 (NF-κB,NRF2/KEAP1).

主要成果:

暴露于MPs引起的突关节损伤,影响了膝关节的形态和功能.
观察到氧化应激增加,亡,结膜纤维化和炎症性细胞因子分泌.
通过对关键炎症标志物进行上调和激活NF-κB和NRF2/KEAP1通路,MPs显著增强了突细胞灭.

结论:

在体内发现表明,MPs暴露通过氧化应激和NF-κB信号传递促进突细胞灭.
MPs破坏突组织结构和功能,可能会加剧SLE的关节损伤.
这项研究在自身免疫性关节疾病的背景下,为微塑料诱导的突关节损伤的机制提供了新的见解.

关键词:

在MRL/lpr小鼠中在NF-κB信号传输中.细胞中发生的高热亡.微塑料微塑料的使用氧化应激是一种氧化应激.综合性炎症综合性炎症

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