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缺血性脑卒中后 NLRP3 炎性小体的激活。

NLRP3 inflammasome activation after ischemic stroke.

机构信息

Department of Sport Rehabilitation, Shanghai University of Sport, Shanghai, China.

Graduate School of Shanghai University of Traditional Chinese Medicine, Shanghai, China.

出版信息

Behav Brain Res. 2023 Aug 24;452:114578. doi: 10.1016/j.bbr.2023.114578. Epub 2023 Jul 11.

DOI:10.1016/j.bbr.2023.114578
PMID:37437697
Abstract

Cerebral ischemia is a pathological condition resulting from the cessation or reduction of blood supply to the cerebral arteries. Neurological deficits that are clinically relevant can arise as a result of brain damage. The etiology of stroke is multifaceted and intricate, with the inflammatory response being a crucial component that warrants significant attention. Following a cerebrovascular accident, the levels of interleukin-1 beta and interleukin-18 within the central nervous system escalate due to the activation of the nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 inflammasome. The inflammation is aggravated by the subsequent occurrence of pyroptosis. The mechanisms that activate the NLRP3 inflammasome pyroptosis signaling pathway axis are described in this article. In addition, we go over how pyroptosis interacts with other processes for regulated cell death. In addition, specific NLRP3 inflammasome pathway inhibitors are identified, which offer new approaches to preventing ischemic brain injury.

摘要

脑缺血是一种由于大脑动脉供血停止或减少而导致的病理状态。由于脑损伤,可能会出现具有临床相关性的神经功能缺损。中风的病因是多方面的,炎症反应是一个关键组成部分,值得高度关注。在脑血管意外后,由于核苷酸结合寡聚结构域样受体家族富含吡啶结构域蛋白 3 炎性小体的激活,中枢神经系统内白细胞介素-1β和白细胞介素-18 的水平升高。随后发生的细胞焦亡使炎症加重。本文描述了激活 NLRP3 炎性小体细胞焦亡信号通路轴的机制。此外,我们还研究了细胞焦亡如何与其他程序性细胞死亡过程相互作用。此外,还确定了特定的 NLRP3 炎性小体通路抑制剂,为预防缺血性脑损伤提供了新的方法。

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