血脑屏障表面葡萄糖转运蛋白1（GLUT1）调节葡萄糖转运入脑。阿尔茨海默病（AD）有着早期葡萄糖转运水平下降现象，伴随着脑血管内皮损伤，血脑屏障表面GLUT1表达下降。病人脑微血管内皮细胞膜上介导β淀粉样蛋白（Aβ）转运的LRP-l表达降低及RAGE表达增加，导致血脑屏障Aβ转运机制异常，从而发生Aβ沉积。临床尚无能有效抑制Aβ沉积的方法，而靶向血管内皮细胞GLUT1清除Aβ则成为新的研究热点。前期研究发现当归芍药散能减少动物脑内Aβ含量，改善血管损伤造成的记忆障碍，这可能与其中有效成分藁本内酯有关。本课题从藁本内酯调节脑血管内皮细胞GLUT1，改善痴呆动物血脑屏障Aβ转运及清除的机制入手，用APP/PS1转基因小鼠、SAMP8快速老化小鼠及Aβ1-42损伤脑微血管内皮细胞模型，结合分子对接方法，分别从体内和体外实验探讨藁本内酯作用于AD的机制，为中医药治疗AD药物研发进行有益的探索与尝试。

The glucose transporter GLUT1 at the blood-brain barrier (BBB) mediates glucose transport into the brain. Alzheimer’s disease is characterized by early reductions in glucose transport associated with dysfunction of brain microvascular endothelial cells (BMEC) and diminished GLUT1 expression at the BBB. A reduction of LRP-1 expression and an overexpression of RAGE in BMEC result in Aβ accumulation and aggregation. There is still no effective drugs to prevent Aβ from accumulation. So clearing Aβ by targeting GLUT1 in BMEC becomes popular. Our preceding research found that Dangdui-Shaoyao-San could decrease the content of Aβ in the brain and improve the memory impairment induced by the dysfunction of brain vascular, which is associated with its effective component, Ligustilide. Our study aims to investigate the effects of Ligustilide on Aβ transport and clearance via regulating GLUT1 in the BMEC of AD Models. APP/PS1 transgenic mice, SAMP8 mice and BMEC treated with Aβ1-42 models were employed in this study. Combined with molecular docking, we explore the mechanism of Ligustilide on AD in vivo and in vitro and provide some evidences of traditional Chinese medicine in the treatment of AD.