Alzheimer’s disease (AD) is a common neurodegenerative disease that is always accompanied by synaptic loss in the brain. Safflower yellow (SY) is the extract of safflower, a traditional Chinese medicine, which has shown neuroprotective effects in recent studies. However, the mechanism of SY in protecting synapses remains unclear. In this study, we are going to study the mechanism of how SY treats AD in terms of synaptic plasticity. We found, via behavioral experiments, that SY treatment could improve the abilities of learning and memory in APP/PS1 mice. In addition, using Golgi staining and HE staining, we found that SY treatment could reduce the loss of dendritic spines in the pathological condition and could maintain the normal physiological state of the cells in cortex and in hippocampus. In addition, the results of immunofluorescence staining and western blotting showed that SY treatment could significantly increase the expression of synapse-related proteins. Moreover, after being treated with SY, the expression of iNOS (marker of M1 microglia) declined remarkably, and the level of Arginase-1 (marker of M2 microglia) increased significantly. Finally, we found BDNF/TrkB/ERK signaling cascade was activated. These results indicate that SY enhances synaptic plasticity in APP/PS1 mice by regulating microglia activation phenotypes and BDNF/TrkB/ERK signaling pathway.

中文翻译：

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红花黄通过调节小胶质细胞激活表型和 BDNF/TrkB/ERK 信号通路改善 APP/PS1 小鼠的突触可塑性。

阿尔茨海默病 (AD) 是一种常见的神经退行性疾病，总是伴随着大脑中的突触丢失。红花黄 (SY) 是中药红花的提取物，在最近的研究中显示出神经保护作用。然而，SY保护突触的机制尚不清楚。在这项研究中，我们将研究SY如何从突触可塑性方面处理AD的机制。我们通过行为实验发现，SY 治疗可以提高 APP/PS1 小鼠的学习和记忆能力。此外，通过高尔基体染色和HE染色，我们发现SY处理可以减少病理状态下树突棘的丢失，并可以维持皮层和海马细胞的正常生理状态。此外，免疫荧光染色和蛋白质印迹结果表明，SY处理可显着增加突触相关蛋白的表达。此外，经SY处理后，iNOS（M1小胶质细胞标志物）的表达显着下降，Arginase-1（M2小胶质细胞标志物）水平显着升高。最后，我们发现 BDNF/TrkB/ERK 信号级联被激活。这些结果表明SY通过调节小胶质细胞活化表型和BDNF/TrkB/ERK信号通路增强APP/PS1小鼠的突触可塑性。并且Arginase-1（M2小胶质细胞的标志物）的水平显着增加。最后，我们发现 BDNF/TrkB/ERK 信号级联被激活。这些结果表明SY通过调节小胶质细胞活化表型和BDNF/TrkB/ERK信号通路增强APP/PS1小鼠的突触可塑性。并且Arginase-1（M2小胶质细胞的标志物）的水平显着增加。最后，我们发现 BDNF/TrkB/ERK 信号级联被激活。这些结果表明SY通过调节小胶质细胞活化表型和BDNF/TrkB/ERK信号通路增强APP/PS1小鼠的突触可塑性。