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.

中文翻译：

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缺血性中风的NLRP3炎性体：可能的治疗靶点。

炎症是中风的毁灭性病理生理过程，是毁灭性疾病，是全球第二大最常见的死亡原因。有人提出激活NOD样受体蛋白（NLRP3）-infammasome来介导缺血性中风期间的炎症反应。简而言之，NLRP3炎性体激活caspase-1，从而将前IL-1和前IL-18裂解为活性的促炎细胞因子，并释放到细胞外环境中。已经开发了几种NLRP3炎性体抑制剂，包括小分子，I型干扰素，微小RNA，一氧化氮和核因子erythroid-2相关因子2（Nrf2），其中一些在临床上可能有效。这篇综述将描述缺血性中风期间NLRP3炎性小体的结构和细胞信号传导途径，