急性脑梗死（ACI）患者存在脑血流自动调节功能（CA）受损，是预后不良的独立危险因素。我们前期研究发现缺血处理可提高健康人和ACI患者的CA，机制与改善血管内皮功能有关；同时发现大脑中动脉闭塞（MCAO）小鼠接受肢体远隔缺血后处理（LRIPoC）后，脑血管内皮细胞SIRT1表达显著升高。SIRT1信号通路有改善血管张力和抗炎功能，具有潜在改善CA的作用。据此我们提出LRIPoC可能通过上调SIRT1表达，进而影响下游eNOS/NO/NLRP3通路来改善ACI后CA的假说。本研究将结合基础和临床研究验证该假说。①动物实验：应用SIRT1基因内皮条件性敲除小鼠，借助免疫荧光、单分子免疫阵列等技术明确LRIPoC对MCAO小鼠静态CA的影响及机制。②临床研究：量化分析LRIPoC对ACI患者动态CA的影响，分析血清SIRT1相关指标与CA的关系。本研究将为LRIPoC治疗ACI提供新的理论依据。

Impaired cerebral autoregulation (CA) is an independent risk factor of the unfavourable prognosis in acute cerebral infarction (ACI) patients. In our previous studies, we found that limb remote ischemic conditioning can increase CA levels in healthy adults and ACI patients, and the mechanism is related to the improvement of endothelial function. Our preliminary experiments also showed that limb remote ischemic postconditioning (LRIPoC) could significantly increase SIRT1 expression in cerebrovascular endothelial cells in middle cerebral artery occlusion (MCAO) mice. SIRT1 signaling pathway has the function of improving vascular tension and anti-inflammation, which may further improve CA. Therefore, we hypothesize that LRIPoC could improve CA after ACI by up-regulating SIRT1 expression and then regulating eNOS/NO/NLRP3 pathway. In this study, we try to verify this hypothesis in two parts. 1. Animal experiments: using immunouorescence staining, single molecule array and other techniques to analyze the effects and mechanism of LRIPoC in improving static CA in brain endothelial conditional SIRT1 knockout MCAO mice. 2. Clinical study: to clarify the effect of LRIPoC on dynamic CA in ACI patients. Simultaneously, protein chip technology will be used to analyze the relationship between serum SIRT1 and downstream indicators and CA. This study will provide a new theoretical basis for the treatment of ACI by LRIPoC.