急性脑梗死（ACI）远隔损害加重神经损伤。课题组近期发现PRG5阻遏LPA/RhoA抑制信号跨膜传导与小胶质细胞炎性因子分泌，电针百会、大椎穴调控RhoA/PRG5减轻黑质、纹状体、海马、脑干远隔损害。但RohA/ROS对NLRP3/caspase-1关键信号通路介导小胶质细胞焦亡致远隔损害有何影响，电针怎样调控NLRP3/caspase-1抑制细胞焦亡减轻远隔损害，这些新的科学问题不清楚。课题用体内、外实验多方位探讨电针介导NLRP3/caspase-1调控小胶质细胞焦亡为新靶点：①沉默NLRP3基因，检测inflammesome相关蛋白caspase-1、NLRP3、ASC，明确细胞焦亡对远隔损害影响及电针作用；②检测IL-1β、IL-18、ROS、RhoA，明确电针对细胞焦亡作用与机制；③观察电针不同时点对神经细胞TUNEL、DNA断裂修复作用，为电针减轻ACI远隔损害提供新理论。

The romote damages of acute cerebral infarction(ACI) aggravated nerve defect. Our team has recently found that PRG5 can downregulate the expression of LPA and RhoA proteins to inhibit the conductance of transmembrane signals and reduce the secretion of inflammatory factors. Electroacupuncture(EA) at Baihui and dazhui could regulate the expressions of RhoA and PRG5 to reduce the remote damages in substantia nigra, corpus striatum, hippocampus and brain stem. However, what about the effect of RhoA/ROS regulating NLRP3/caspase-1key signaling pathway mediated microglial pyroptosis for remote damages? How does EA to regulate NLRP3/caspase-1 signaling pathway inhibiting microglial pyroptosis to alleviate remote damages? Above scientifically new questions are still unclear. Our team will use vivo and vitro experiments to study the novel target that EA can induce remote damages of ACI by regulating NLRP3/caspase-1 signaling pathway in multi perspective: ① we will examine the expression of caspase-1, NLRP3, ASC in remote areas after siRNA-mediated silencing of NLRP3, the influence of pyroptosis in remote areas and the effect of EA would be assessed. ② we will detect the expression of IL-1β, IL-18, ROS, RhoA,and LPA, and the mechanism of EA on pyroptosis would be studied. ③ we will observe the influence of EA on cell death/nuclear shrinkage, DNA fragmentation and nerve repair in differet times of ACI remote areas, and we may provide the novel theory of EA on ACI remote damages.