前期研究显示，红花黄色素（SY）可明显改善不同类型痴呆动物的学习记忆能力，抑制β淀粉样蛋白沉积的同时增加突触素的表达，抑制胶质纤维酸性蛋白的表达，对神经元具有一定的保护作用。为进一步明确SY是否通过减轻Aβ对突触可塑性损伤而发挥防治AD的作用？或是抑制Aβ对胶质细胞的活化作用，减轻随后的神经炎症反应而发挥其学习记忆改善作用？本课题以突触可塑性和胶质细胞活化为研究靶点，采用APP/PS1转基因小鼠及Aβ1-42海马注射致大鼠痴呆模型，观察SY对突触传递的长时程增强、突触形态、数量、突触相关蛋白表达及突触可塑性调节机制的影响。观察SY对胶质细胞活化、炎症介质释放及胶质细胞炎症形态的影响。在细胞水平，建立神经元及神经元与胶质细胞共培养体系，观察SY对Aβ1-42处理的细胞培养体系突触毒性的影响，进一步明确SY调节突触可塑性的分子机制，希望能寻找一种可延缓AD发病进程的药物。

Previous studies showed that safflor yellow (SY) improved the learning and memory deficits in different dementia model, inhibited amyloid deposit and glial fibrillary acidic portein expression, increased the expression of synaptophysin and protected the neuron. In order to further determine whether SY exert the therapeutical effect for AD by reducing Aβ induced synaptic plasticity damage? Or SY exert the effect of learning and memory improvement by inhibiting Aβ induced glia activation, reducing subsequent nerve inflammation? On this topic, we will take the synaptic plasticity and glia activation as the research target, using APP/PS1 transgenic mice and Aβ1-42 hippocampus-injected rats to further observe the regulatory role of SY on long-term potentiation, synaptic morphology, synaptic number, synapse-associated proteins expression and the regulatory mechanism. We will also observe the regulatory effects of SY on glia activation, secretion of inflammatory mediator and the inflammatory morphology of glia. At the cellular level, we will observe the effect of SY on synaptic toxicity in neuron and the coculture system of neuron and glia of Aβ1-42 treatment.This cellular experiment is used to further investigate the regulatory mechanisme of SY on synaptic plasticity. This project is expected to find a drug to delay the process of Alzheimer's disease.