电针刺激预处理（EAP）可减轻随后发生的脑缺血损害，其脑保护作用可能与减轻中枢神经系统（CNS）炎症反应有关，但其关键分子尚不清楚。小胶质细胞的活化状态（M1/M2）对于神经炎症的调节至关重要，而髓样细胞表达的激发受体II型受体（TREM2）分布于小胶质细胞，是调节小胶质细胞活化状态的关键靶点。我们的预试验表明，EAP可上调TREM2的表达，而TREM2激动剂HSP60可产生与EAP相似的脑保护效应。本研究拟从分子、细胞和整体动物等多层面，以TREM2为切入点，采用免疫双标、siRNA干扰和转基因小鼠等研究方法，研究EAP是否通过调控TREM2进而使激活的小胶质细胞从M1状态向M2状态转化，抑制CNS炎症，减轻继发性损伤。将为进一步明确EAP的关键分子和机制提供新的理论依据，也为防治CNS炎症反应过度引起的继发性损伤提供了新靶点。

Electroacupuncture preconditioning (EAP) protects the brain against the subsequent ischemic injury. Alleviated neuroinflammation plays a role in it but the essential modulator remains unclear. Type II bone marrow cells activated receptor (TREM2) is expressed on microglia and could negatively regulate the excessive activation of microglia and the process of inflammation. Our pilot study showed that EAP could upregulate the level of TREM2, which may drive the microglia transforming from M1 state to M2 state. And TREM2 agonist HSP60 could induce similar cerebral protection as EAP. These evidences strongly indicate that TREM2 could be the target of EAP modulating neuroinflammation. In this study, we tend to investigate the effect of EAP modulated by TREM2 through regulating microglia activation, using methods including siRNA interference, immunofluorescence labeling and knockout mice. We aim to clarify the role of TREM2 in EAP, to explore the essential mechanism of EAP, and thus to find new target for preventing excessive neuroinflammation induced brain damage.