脑卒中已成为威胁我国人群第一致死原因，炎症反应是其神经损伤的关键环节，但相关的调控机制尚不明确。本课题组前期研究发现，脑卒中后胶质细胞NLRP3炎症小体激活，脂联素及其受体通路发挥显著的抑炎作用，我们提出“NLRP3炎症小体的激活是脑卒中后神经炎症损伤的重要机制，脂联素及其受体通过调控NLRP3炎症小体通路抑制神经炎症，在脑卒中后发挥神经保护作用。”基于以上假说，本课题拟以多种脑卒中模型为基础，综合运用神经形态学、分子生物学、神经机能学、药理学等实验方法，首先明确脂联素及其受体对脑卒中后胶质细胞及炎症反应的作用；深入研究NLRP3炎症小体的激活与脑卒中后神经炎症损伤的相关性，从一个全新的角度阐明脑卒中后神经损伤的炎症机制；并观察脂联素及其受体信号通路对NLRP3炎症小体的调控作用，有望发现以脂联素为基础的新的神经炎症干预靶点，从而为临床治疗脑卒中提供新的理论基础和实验依据。

Stroke has been the number one killer in our country. The inflammation reaction plays a pivotal role in ischemic stroke, but the underlying mechanisms remain exclusive. Our previous results suggest that the NLRP3 inflammasome activation in astrocytes and adiponectin (APN) confers significant anti-inflammatory effect. Therefore, we propose that NLRP3 inflammasome activation is the important mechanism involved in brain injury after stroke and APN inhibits inflammation by regulating NLRP3 inflammasome. The present study plans to evaluate the effect of APN and APN receptors on astrocytes after stoke and inflammation and to investigate the relation between NLRP3 inflammasome activation and neuroinflammation after stroke. In addition, we want to investigate how APN regulates NLRP3 inflammasome and this study will provide new theoretical and experimental foundations for the treatment of stroke.