血管性痴呆(VaD)是指各种脑血管病引起的获得性智能损害和认知障碍综合征，发病机制不明确。免疫功能和炎症反应与VaD密切相关，我们研究发现，穴位埋线(CIAA)可降低VaD大鼠IL-1β，TNF-α含量，改善学习记忆，但VaD与免疫功能、炎症反应的相关性仍需深入研究。TLR4属于模式识别受体，MyD88是TLR4通路中关键的衔接蛋白，能够启动下游炎性因子的转导，TLR4/MyD88通路可介导炎症反应，加重脑缺血损伤。CIAA改善VaD的症状是否与TLR4/MyD88通路有关尚不清楚。我们假说CIAA改善VaD大鼠学习记忆的机理与其负向调控TLR4/MyD88通路介导炎症反应、调整免疫功能有关。为验证该假说，本项目基于神经免疫学，采用PCR、WB等手段，从细胞和分子水平，探索CIAA改善VaD学习记忆与TLR4/MyD88通路介导炎症反应的关系，研究CIAA改善VaD学习记忆的机制。

Vascular dementia (VaD) is a syndrome of acquired intellectual impairment and cognitive impairment caused by various cerebrovascular diseases,The pathogenesis is unclear.Immune function and inflammatory response are closely related to VaD.Our study found that catgut implantation at acupoint(CIAA）can reduce the content of IL-1β and TNF-α in VaD rats,and improve the learning and memory abilities of VaD rats,but the correlation between VaD and immune function and inflammatory response still needs further study.TLR4 belongs to pattern recognition receptor,MyD88 is the key adapter protein in TLR4 pathway, which can initiate downstream inflammatory factors conduction.TLR4/My D88 pathway can mediate inflammatory reaction and aggravate the damage of cerebral ischemia.However,It is not clear whether the improvement of VaD symptoms by CIAA is related to the TLR4/MyD88 pathway.we hypothesized that the mechanism of learning and memory was improved with CIAA in VaD rats which is related to the negative regulation of TLR4/ MyD88 pathways mediate inflammation reaction and adjust immune function.In order to verify this hypothesis,this project base on neuroimmunology,use the means of PCR、Western blotting and other means,from the cellular and molecular levels, explore the relation between CIAA improving the learning and memory of VaD rats and TLR4/MyD88 pathways mediate inflammation reaction,study the mechanism of learning and memory was improved with CIAA in VaD rats.