脑水肿是导致大面积脑梗死死亡和重度残疾的重要因素。我们前期研究提示梗死后脑水肿患者血浆中Cathepsin B表达增高，其他疾病研究提示Cathepsin B可通过NLRP3炎性小体导致炎症反应。故我们提出研究假设：大面积脑梗死发生后Cathepsin B表达增高从而激活NLRP3炎性小体介导的炎症反应导致脑水肿形成。本研究拟在前期基础上：1）通过大鼠脑梗死模型，探索Cathepsin B和NLRP3表达与脑水肿发生及严重度的关系，并逐步抑制Cathepsin B及NLRP3，以探明该通路序贯激活对脑水肿的影响；2）观察脑梗死患者针刺后Cathepsin B及NLRP3炎性小体表达变化及脑水肿发生严重度，明确可否通过下调Cathepsin B与NLRP3炎性小体表达水平减轻脑梗死后水肿。本研究旨在探明大面积脑梗死后脑水肿发生的分子机制并进行临床验证，为其早期预防或干预提供新的理论机制。

Cerebral edema is one of the most important causes of death and disability after large hemispheric infarction. Our previous study has suggested that the expression of plasma Cathepsin B increased in patients with cerebral edema. Studies of other diseases have indicated that Cathepsin B might activate NLRP3 inflammasome and cause inflammatory reactions. Therefore, we propose a hypothesis that the increase in Cathepsin B expression after large hemispheric infarction activates NLRP3 inflammasome, leading to the development of cerebral edema. We plan 1. to explore the association of the expression of Cathepsin B and NLRP3, with the occurrence and severity of cerebral edema in the MCAO rat models, and detect the influence of the pathway on cerebral edema by gradually inhibiting Cathepsin B and NLRP3 inflammasome; 2. to evaluate the expression changes of Cathepsin B and NLRP3 inflammasome, and the severity of cerebral edema of patients with cerebral infarction after receiving acupuncture; and whether the edema can be reduced by down-regulating the expression levels of Cathepsin B and NLRP3 inflammasome. The purpose of this study is to investigate and validate the molecular mechanisms of brain edema after large hemispheric infarction, and providing a new theoretical target for the early prevention of cerebral edema after stroke.