甘露聚糖结合凝集素（MBL）补体活化途径在脑缺血损伤中发挥重要作用。申请人研究发现：急性缺血性脑卒中患者MBL水平显著性增高，并且与患者NIHSS得分呈正相关；预实验结果显示：电针预处理可下调缺血再灌注小鼠MBL水平，MBL基因敲除小鼠脑缺血后TLR4表达下调。有研究发现：MBL对TLR信号转导通路具有调节作用。综上，我们提出本课题假说：电针预处理引起MBL表达下调，抑制脑缺血后MBL激活TLR4，进而通过干预TLR4-MyD88-NF-kB信号传导途径，减少脑缺血再灌注后促炎因子的表达和细胞凋亡，激活内源性保护机制，诱导脑保护效应。本课题拟以MBL基因敲除小鼠和TLR4基因敲除小鼠为平台，采用免疫组化、免疫荧光、Western blot、实时定量PCR等方法，深入研究电针预处理抑制脑缺血后MBL激活TLR4的机制，为脑缺血损伤防治提供新的理论依据，体现针灸治未病理念。

Complement activation have been suggested in the pathogenesis of stroke, mannose-binding lectin (MBL) were found to plays an important role during the process. Our studies demonstrate that the serum MBL levels were significantly higher in acutely ischemic stroke patients as compared to normal controls.There was a correlation between serum levels of MBL and NIHSS score. Our most recent pilot studies demonstrate that electroacupuncture (EA) preconditioning inhibites MBL after cerebral ischemia. The expression of TLR4 in MBL knockout mice decreased. We therefore put forward the central hypothesis of this project: EA preconditioning-induced decrease of MBL and consequent activation of TLR4 signaling, inhibites TLR4-MyD88-NF-kB signaling and consequently decrease inflammatory and apoptosis, induce neuronal tolerance neuroprotection. We will test this hypothesis with ischemic model on MBL knockout mice and TLR4 knockout mice, using Immunohistochemical and Immunofluorescense,Western blot,Real time PCR,to detect the mechanism of EA preconditioning inducing the inhibition of MBL and consequent activation of TLR4 signaling after cerebral ischemia. These novel studies will provide a novel solid base on stroke treatment.