AIM Alzheimer's disease (AD), a neurodegenerative disease, is characterized by memory loss and synaptic damage. Up to now, there are limited drugs to cure or delay the state of this illness. Recently, the Fyn tyrosine kinase is implicated in AD pathology triggered by synaptic damage. Thus, Fyn inhibition may prevent or delay the AD progression. Therefore, in this paper, we investigated whether Panaxadiol could decrease synaptic damage in AD and the underlying mechanism. MAIN METHODS The ability of learning and memory of mice has detected by Morris Water Maze. The pathological changes detected by H&E staining and Nissl staining. The percentage of cell apoptosis and the calcium concentration were detected by Flow Cytometry in vitro. The amount of synaptic protein and related proteins in the Fyn/GluN2B/CaMKIIα signaling pathway were detected by Western Blot. KEY FINDINGS In the present article, Panaxadiol could significantly improve the ability of learning and memory of mice and reduce its synaptic dysfunction. Panaxadiol could down-regulate GluN2B's phosphorylation level by inhibition Fyn kinase activity, Subsequently, decrease Ca2+-mediated synaptic damage, reducing LDH leakage, inhibiting apoptosis in AD, resulting in facilitating the cells survival. For the underlying molecular mechanism, we used PP2 to block the Fyn/GluN2B/CaMKIIα signaling pathway. The results from WB showed that the expression of related proteins in the Fyn signaling pathway decreased with PP2 treated. SIGNIFICANCE Our results indicate that Panaxadiol could decrease synaptic damage, which will cause AD via inhibition of the Fyn/GluN2B/CaMKIIα signaling pathway. Thus, the Panaxadiol is a best promising candidate to test as a potential therapy for AD.

中文翻译：

---

人参二醇抑制阿尔茨海默氏病中的突触功能障碍，并靶向APP / PS1小鼠和APP-SH-SY5Y细胞中的Fyn蛋白。

AIM阿尔茨海默氏病（AD）是一种神经退行性疾病，其特征在于记忆力减退和突触损伤。迄今为止，治疗或延缓这种疾病状态的药物有限。最近，Fyn酪氨酸激酶与突触损伤触发的AD病理学有关。因此，Fyn抑制可预防或延迟AD进展。因此，在本文中，我们研究了人参二醇是否可以减少AD中的突触损伤及其潜在机制。主要方法Morris Water Maze已检测出小鼠的学习和记忆能力。通过H＆E染色和Nissl染色检测病理变化。流式细胞术检测细胞凋亡百分比和钙浓度。Western Blot检测Fyn / GluN2B /CaMKIIα信号通路中突触蛋白和相关蛋白的量。主要发现在本文中，人参二醇可以显着提高小鼠的学习和记忆能力，并减少其突触功能障碍。人参二醇可以通过抑制Fyn激酶的活性来下调GluN2B的磷酸化水平，进而减少Ca2 +介导的突触损伤，减少LDH的泄漏，抑制AD的凋亡，从而促进细胞的存活。对于潜在的分子机制，我们使用PP2阻断Fyn / GluN2B /CaMKIIα信号传导途径。WB的结果表明，用PP2处理后，Fyn信号通路中相关蛋白的表达降低。意义我们的结果表明人参二醇可以减少突触损伤，会通过抑制Fyn / GluN2B /CaMKIIα信号传导途径引起AD。因此，人参二醇是测试作为AD的潜在疗法的最有希望的候选者。