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Prdx6 调节Nlrp3 炎症酶激活驱动的炎症反应在镜片上皮细胞

Bhavana Chhunchha¹, Rakesh Kumar¹, Eri Kubo²

¹Department of Ophthalmology and Visual Sciences, University of Nebraska Medical Center, Omaha, NE 68198, USA.

International journal of molecular sciences

|November 25, 2023

概括

过氧化素6 (Prdx6) 缺乏导致氧化应激和Nlrp3炎症酶激活,导致衰老细胞的炎症和热. 恢复Prdx6或减少ROS可以防止这种炎症过程.

科学领域:

细胞和分子生物学细胞和分子生物学
免疫学免疫学免疫学
衰老研究研究衰老研究

背景情况:

抗氧化剂反应失调和NLRP3炎症酶激活与衰老和氧化应激有关.
氧化素6 (Prdx6) 是一种关键的抗氧化剂,通过维持氧化还原平衡,保护细胞.

研究的目的:

调查Prdx6在调节氧化压力驱动的Nlrp3炎症酶激活和老化的镜片上皮细胞 (LEC) 中的热的作用.

主要方法:

使用了Prdx6-缺乏 (Prdx6-/-) 和老化的LEC,以及老化的镜片.
评估了反应性氧物种 (ROS) 水平,Nlrp3炎症组分 (Caspase-1,IL-1β,ASC,Gasdermin-D) 和克鲁佩尔类因子9 (Klf9) 表达.
研究了Prdx6传递和Klf9沉默对炎症反应的影响.

主要成果:

在LEC中Prdx6缺乏和衰老导致ROS积累增加和Nlrp3炎症酶激活增加.
氧化应激放大了ROS和NLRP3通路的激活,类似于脂多糖治疗.
在Prdx6-/-和老化的LEC中,Klf9表达因氧化应激而升级,从而驱动Nlrp3转录. 通过Prdx6输送或Klf9沉默消除ROS抑制了炎症.

结论:

Prdx6作为一个内在的检查点,控制老化和氧化还原活性LECs中的细胞健康.
Prdx6 缺乏会促进氧化应激诱导的 Nlrp3 炎症酶激活和烧灭.
向Prdx6或Klf9为由异常NLRP3炎症酶激活驱动的氧化/衰老相关疾病提供了潜在的治疗策略.

关键词:

在Caspase-1中,GSDMDMD的总体发展目标是什么一个IL-1ββ.NF-BB 这是一个很好的方法.在 Nlrp3 中,过氧化素 6 过氧化素 6 氧化应激是一种氧化应激.

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