相关实验视频

Updated: May 17, 2025

Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1β in Human Monocyte-derived Dendritic Cells

Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1β in Human Monocyte-derived Dendritic Cells

Published on: May 22, 2014

在酸诱导的肌肉神经炎症中,MLKL触发了NLRP3的激活

Yixin Cui¹, Meng Zhang¹, Yi Xiao²

¹School of Public Health, Xi'an Jiaotong University Health Science Center, NHC Key Laboratory of Environment and Endemic Diseases, National Health Commission of the People's Republic of China, No. 76 Yanta West Road, Xi'an, Shaanxi 710061, PR China.

|April 6, 2025

概括

暴露会通过激活混合基因酶域样蛋白 (MLKL) 引起心脏损伤,从而触发NLRP3炎症体. 抑制MLKL可以防止这种引起的心肌神经炎症.

科学领域:

心血管毒理学心血管毒理学
细胞死亡的分子机制
炎症有一些生物学.

背景情况:

暴露与心血管疾病有关,但心肌损伤的潜在机制尚未完全理解.
以前的研究表明,污染的水会在老鼠心肌中引起炎症和死亡损伤.
混合基因酶域样蛋白 (MLKL) 在诱导的心肌性脑炎症中的作用需要阐明.

研究的目的:

为了调查MLKL激活是否会触发样受体蛋白-3 (NLRP3) 在诱导的心肌性脑炎炎症中的炎症酶激活.
检查死抑制剂和MLKL遗传淘汰对诱导的心脏损伤的保护作用.
为了确定RIPK3/MLKL通路在引起的心肌损伤中的参与.

主要方法:

使用了H9C2心肌细胞和Mlkl淘汰C57BL/6小鼠模型.
用于诱导心肌损伤的暴露.
采用了亡抑制剂 (Necrostatin-1,GSK-872,NSA) 和MLKL遗传淘汰.
评估了NLRP3炎症组分 (NLRP3,Caspase-1,IL-1β) 的表达.

主要成果:

暴露通过RIPK3/MLKL途径在体外和体内诱导了亡.
死亡抑制剂和MLKL淘汰对引起的炎症损伤进行了部分保护.
这些干预措施降低了关键的NLRP3炎症酶蛋白,包括NLRP3,Caspase-1和IL-1β.

结论:

混合基因酶域样蛋白 (MLKL) 的激活是诱导的心肌炎症的一个关键事件.
MLKL触发NLRP3炎症酶激活,导致引起的心脏损伤.
针对MLKL/NLRP3轴可能为与有关的心血管毒性提供治疗策略.

关键词:

亚是一种.一个心肌细胞.在心肌中,心肌.骨髓炎的炎症骨髓炎尸体灭 (Necroptosis) 是一种死亡的过程.

更多相关视频

Detection of Inflammasome Activation and Pyroptotic Cell Death in Murine Bone Marrow-derived Macrophages

Detection of Inflammasome Activation and Pyroptotic Cell Death in Murine Bone Marrow-derived Macrophages

Published on: May 21, 2018

Characterization of MLKL-mediated Plasma Membrane Rupture in Necroptosis

Characterization of MLKL-mediated Plasma Membrane Rupture in Necroptosis

Published on: August 7, 2018

相关概念视频

NF-κB-dependent Signaling Pathway

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...