Cerebrovascular diseases are pathological conditions involving impaired blood flow in the brain, primarily including ischaemic stroke, intracranial haemorrhage, and subarachnoid haemorrhage. The nucleotide-binding and oligomerisation (NOD) domain-like receptor (NLR) family pyrin domain (PYD)-containing 3 (NLRP3) inflammasome is a protein complex and a vital component of the immune system. Emerging evidence has indicated that the NLRP3 inflammasome plays an important role in cerebrovascular diseases. The function of the NLRP3 inflammasome in the pathogenesis of cerebrovascular diseases remains an interesting field of research. In this review, we first summarised the pathological mechanism of cerebrovascular diseases and the pathological mechanism of the NLRP3 inflammasome in aggravating atherosclerosis and cerebrovascular diseases. Second, we outlined signalling pathways through which the NLRP3 inflammasome participates in aggravating or mitigating cerebrovascular diseases. Reactive oxygen species (ROS)/nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), ROS/thioredoxin-interacting protein (TXNIP) and purinergic receptor-7 (P2X7R) signalling pathways can activate the NLRP3 inflammasome; activation of the NLRP3 inflammasome can aggravate cerebrovascular diseases by mediating apoptosis and pyroptosis. Autophagy/mitochondrial autophagy, nuclear factor E2-related factor-2 (Nrf2), interferon (IFN)-β, sirtuin (SIRT), and phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) reportedly alleviate cerebrovascular diseases by inhibiting NLRP3 inflammasome activation. Finally, we explored specific inhibitors of the NLRP3 inflammasome based on the two-step activation of the NLRP3 inflammasome, which can be developed as new drugs to treat cerebrovascular diseases.

脑血管疾病是涉及大脑血流受损的病理状况，主要包括缺血性中风、颅内出血和蛛网膜下腔出血。核苷酸结合和寡聚化 (NOD) 结构域样受体 (NLR) 家族 pyrin 结构域 (PYD) 包含 3 (NLRP3) 炎症小体是一种蛋白质复合物，是免疫系统的重要组成部分。新的证据表明 NLRP3 炎症小体在脑血管疾病中起重要作用。NLRP3 炎症小体在脑血管疾病发病机制中的作用仍然是一个有趣的研究领域。本文首先综述了脑血管疾病的病理机制以及NLRP3炎症小体加重动脉粥样硬化和脑血管疾病的病理机制。第二，我们概述了 NLRP3 炎症小体参与加重或减轻脑血管疾病的信号通路。活性氧 (ROS)/活化 B 细胞的核因子 kappa-轻链增强子 (NF-κB)、ROS/硫氧还蛋白相互作用蛋白 (TXNIP) 和嘌呤能受体-7 (P2X7R) 信号通路可以激活 NLRP3 炎症小体; NLRP3炎症小体的激活可通过介导细胞凋亡和细胞焦亡加重脑血管疾病。自噬/线粒体自噬、核因子 E2 相关因子-2 (Nrf2)、干扰素 (IFN)-β、沉默调节蛋白 (SIRT) 和磷酸肌醇 3-激酶 (PI3K)/蛋白激酶 B (AKT) 据报道通过抑制NLRP3 炎症小体激活。最后，