Fibrauretine is the main active ingredient in rattan stems of Fibraurea recisa Pierre. The aim of this study was to evaluate the cognitive-enhancing effects and underlying molecular mechanisms of fibrauretine compatibilized with ginsenosides on Alzheimer's disease (AD) induced in mice with amyloid β-protein (Aβ1-42). The results showed that the spatial learning and memory abilities of AD mice were significantly enhanced after combined treatment with fibrauretine and ginsenosides using the Morris water maze test. The levels of acetylcholinesterase (AChE) and phosphorylated Tau protein (p-Tau) in brain tissue and the levels of nitric oxide (NO), malondialdehyde (MDA), and N-terminal pro-brain natriuretic peptide (NT-proBNP) in plasma were significantly increased in Aβ1-42-induced AD mice, and these effects were reversed after combined treatment with fibrauretine and ginsenosides. By contrast, a significant increase in the levels of catalase (CAT), superoxide dismutase (SOD), choline acetyltransferase (ChAT) and glutathione peroxidase (GSH-Px) was observed in the combined treatment group. The results of haematoxylin and eosin (H&E) staining, terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labelling (TUNEL) analysis, immunohistochemistry (IHC) and Western blot analysis showed that the apoptosis rate, Bax, nuclear factor kappa-B p65 (NF-κBp65), cleaved caspase-3 and cleaved caspase-9 expression levels were obviously decreased and that the Bcl-2 expression levels were significantly increased in the hippocampi of mice treated with fibrauretine and ginsenosides. The results of this study show that the ameliorative effect of fibrauretine against AD can be significantly enhanced by compatibilization with ginsenosides. The underlying molecular mechanisms of fibrauretine may be related to antioxidation and anti-apoptosis.

中文翻译：

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通过与人参皂苷增容，纤维脲素对 Aβ1-42 诱导的阿尔茨海默病的认知增强作用

Fibrauretine 是 Fibraurea recisa Pierre 藤茎中的主要活性成分。本研究的目的是评估与人参皂苷相容的纤维脲素对β淀粉样蛋白 (Aβ1-42) 小鼠诱导的阿尔茨海默病 (AD) 的认知增强作用和潜在分子机制。Morris水迷宫试验结果表明，纤维脲素和人参皂苷联合治疗后，AD小鼠的空间学习记忆能力显着增强。脑组织中乙酰胆碱酯酶 (AChE) 和磷酸化 Tau 蛋白 (p-Tau) 的水平以及血浆中一氧化氮 (NO)、丙二醛 (MDA) 和 N 端脑钠肽前体 (NT-proBNP) 的水平在 Aβ1-42 诱导的 AD 小鼠中显着增加，并且这些作用在与纤维脲素和人参皂苷联合治疗后被逆转。相比之下，在联合治疗组中观察到过氧化氢酶 (CAT)、超氧化物歧化酶 (SOD)、胆碱乙酰转移酶 (ChAT) 和谷胱甘肽过氧化物酶 (GSH-Px) 的水平显着增加。苏木精伊红（H&E）染色、末端脱氧核苷酸转移酶介导的dUTP-生物素缺口末端标记（TUNEL）分析、免疫组化（IHC）和Western blot分析结果显示，细胞凋亡率、Bax、核因子κ-B p65（ NF-κBp65)、cleaved caspase-3 和cleaved caspase-9 表达水平明显降低，Bcl-2 表达水平在用纤维脲素和人参皂苷处理的小鼠海马中显着增加。本研究的结果表明，通过与人参皂苷的增容可以显着增强纤维脲素对 AD 的改善作用。纤维脲素的潜在分子机制可能与抗氧化和抗细胞凋亡有关。