期刊
INTERNATIONAL JOURNAL OF STROKE
卷 14, 期 6, 页码 574-591出版社
SAGE PUBLICATIONS LTD
DOI: 10.1177/1747493019841242
关键词
Ischemic stroke; inflammation; NLRP3 inflammasome; small molecule; interferon; micro RNA; nitric oxide; Nrf2
Inflammation is a devastating pathophysiological process during stroke, a devastating disease that is the second most common cause of death worldwide. Activation of the NOD-like receptor protein (NLRP3)-infammasome has been proposed to mediate inflammatory responses during ischemic stroke. Briefly, NLRP3 inflammasome activates caspase-1, which cleaves both pro-IL-1 and pro-IL-18 into their active pro-inflammatory cytokines that are released into the extracellular environment. Several NLRP3 inflammasome inhibitors have been promoted, including small molecules, type I interferon, micro RNAs, nitric oxide, and nuclear factor erythroid-2 related factor 2 (Nrf2), some of which are potentially efficacious clinically. This review will describe the structure and cellular signaling pathways of the NLRP3 inflammasome during ischemic stroke, and current evidence for NLRP3 inflammasome inhibitors.
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