本课题拟采用大脑中动脉阻塞法建立小鼠局灶性脑缺血再灌注损伤模型，并通过细胞糖氧剥夺法建立小鼠脑微血管内皮细胞和小胶质细胞缺血（氧）再灌注损伤模型，分别应用基因沉默和基因过表达技术抑制或增加p120的基因表达，通过行为学、形态学、分子生物学、免疫荧光共聚焦、免疫沉淀等方法，深入探讨脑缺血再灌注损伤后p120的动态变化，阐明其对脑缺血再灌注损伤后炎症的保护作用是通过负向调控TLR4信号通路实现的，深入研究调控p120表达水平的相关细胞信号转导途径，证明与TLR-4及Calpain蛋白激酶的活性有关。最终达到明确p120在脑缺血再灌注损伤后炎症反应中的作用和作用机制的目的，充实和完善脑缺血再灌注损伤的分子生物学机制，并为研究防治缺血性脑血管疾病的药物提供新的作用靶点，具有重要的理论意义和应用价值。

The topic will establish focal cerebral ischemia and reperfusion injury model in mice by using the middle cerebral artery occlusion method as well as mouse brain microvascular endothelial cells and microglia of ischemia and re-reperfusion injury model through the cellular oxygen-glucose deprivation. Respectively, application of gene silencing and gene overexpression to suppress or increase the p120 gene expression, through behavior, morphology, molecular biology, immunofluorescence cofocal image and immunoprecipitation methods, we deeply explore p120 dynamic changes after cerebral ischemia and reperfusion injury to clarify the protective effect of p120 on inflammation by negatively regulate TLR4 signaling pathway, in-depth to investigate the cell signal transduction pathways of the regulation of p120 expression which is proved related to the TLR4 and calpain protein kinase activity. Ultimately, make clear that the roles and mechanisms of p120 in cerebral ischemia and reperfusion injury induced inflammation, which will enrich molecular biological mechanisms of cerebral ischemia and reperfusion injury, and provide the new target for prevention and treatment of ischemic cerebrovascular disease drugs, which has important theoretical significance and application value.