Alzheimer’s disease (AD) is a common neurodegenerative disease, always clinically manifesting with memory loss and other cognitive abilities serious enough to interfere with daily life. Over the past decade, the extensive accumulation of Aβ plaques and the related neuroinflammation such as the activation of glial cells have been frequently demonstrated to contribute to the pathogenesis of AD. However, drugs promoting Aβ plaques degradation and modulating the neuroinflammation remain undeveloped for AD treatment. Mulberry (or Morus alba Linn.) fruit, a common folk medicine, has been demonstrated to exhibit a considerable neuroprotective effect such as promoting memory impairment and enhancing cognitive ability on Parkinson’s-disease-related animal models. Whether mulberry fruit can treat or alleviate AD-related symptoms are unclear so far. In the present study, we estimated the neuroprotective effects of mulberry fruit ethanol extract (MFE) using APP/PS1 transgenic mice, a widely used AD animal model. We found that daily oral MFE (100 mg/kg body weight, for 1.5–3 weeks) remarkably improved the spatial memory and learning ability of APP/PS1 mice, determined by behavioral tests including the Rotarod, Elevated plus maze and Morris water maze test. In histological, we observed that MFE reduced Aβ plaques and neuron apoptosis both in the cortex and hippocampus tissues of APP/PS1 mice. Moreover, MFE treatment noticeably alleviated the neuroinflammation, indicated by the decreased number of astrocytes in the cortex and hippocampus of APP/PS1 mice. These results were further confirmed by the elevation of anti-inflammatory cytokines (IL-4) and reduction of pro-inflammatory cytokines (IL-1β, IL-6 and TNF-α) in the cortex and hippocampus tissues of MFE-treated APP/PS1 mice. Collectively, our findings demonstrate that MFE exhibits a good neuroprotective effect on APP/PS1 mice. Therefore, MFE may be a promising therapeutic drug in the treatment of neurodegenerative disorders, especially like AD.

阿尔茨海默氏病（AD）是一种常见的神经退行性疾病，在临床上总是表现为记忆丧失和其他严重影响日常生活的认知能力。在过去的十年中，Aβ斑块的大量积累和相关的神经炎症（例如神经胶质细胞的激活）已被证明有助于AD的发病。然而，用于AD治疗的促进Aβ斑块降解和调节神经炎症的药物仍未开发。桑（或桑）Linn。）水果是一种常见的民间药物，已被证明对帕金森氏病相关的动物模型具有显着的神经保护作用，如促进记忆力受损和增强认知能力。到目前为止，尚不清楚桑can果是否可以治疗或缓解AD相关症状。在本研究中，我们使用广泛使用的AD动物模型APP / PS1转基因小鼠评估了桑树果实乙醇提取物（MFE）的神经保护作用。我们发现，每天的口服MFE（100 mg / kg体重，持续1.5–3周）可以显着改善APP / PS1小鼠的空间记忆和学习能力，这是通过行为测试（包括Rotarod，高架迷宫和Morris水迷宫测试）确定的。在组织学上，我们观察到MFE减少了APP / PS1小鼠的皮质和海马组织中的Aβ斑块和神经元凋亡。此外，MFE治疗显着减轻了神经炎症，这是由APP / PS1小鼠的皮质和海马中星形胶质细胞数量减少所表明的。通过MFE处理的APP /的皮层和海马组织中抗炎细胞因子（IL-4）的升高和抗炎细胞因子（IL-1β，IL-6和TNF-α）的降低进一步证实了这些结果。 PS1小鼠。总的来说，我们的发现表明MFE对APP / PS1小鼠表现出良好的神经保护作用。因此，MFE可能是治疗神经退行性疾病（尤其是AD）的有前途的治疗药物。通过MFE处理的APP /的皮层和海马组织中抗炎细胞因子（IL-4）的升高和抗炎细胞因子（IL-1β，IL-6和TNF-α）的降低进一步证实了这些结果。 PS1小鼠。总的来说，我们的发现表明MFE对APP / PS1小鼠表现出良好的神经保护作用。因此，MFE可能是治疗神经退行性疾病，尤其是AD的有前途的治疗药物。通过MFE处理的APP /的皮层和海马组织中抗炎细胞因子（IL-4）的升高和抗炎细胞因子（IL-1β，IL-6和TNF-α）的降低进一步证实了这些结果。 PS1小鼠。总的来说，我们的发现表明MFE对APP / PS1小鼠表现出良好的神经保护作用。因此，MFE可能是治疗神经退行性疾病，尤其是AD的有前途的治疗药物。