Rationale

Amyloid β peptide (Aβ) triggers a series of pathological events including microglial activation, oxidative stress, and inflammation-causing neuronal death and typical pathological changes in Alzheimer’s disease (AD).

Objectives

This study aimed to investigate the therapeutic effects and mechanism of bulbocodin D for AD in vivo.

Methods

In this study, Morris water maze (MWM) analysis was used to detect the cognitive ability of APP/PS1 mice after gavage with bulbocodin D for 2 months. Levels of Aβ40, Aβ42, IL-1β, and TNF-α were evaluated by ELISA. Aβ plaques and biomarkers of neuroinflammation were also investigated through histological analysis.

Results

We established that bulbocodin D significantly improved cognitive deficits in APP/PS1 transgenic mice and reduced the levels of amyloid plaque, Aβ40, and Aβ42. Bulbocodin D also reduced levels of microglial markers IbA1, GFAP, and antioxidant enzymes and reduced the products of lipid peroxidation and proinflammatory cytokines.

Conclusion

In summary, the present study provides preclinical evidence that oral bulbocodin D can reduce AD pathology.

中文翻译：

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Bulbocodin D通过调节β-淀粉样蛋白的负担，氧化状态和神经炎症来改善APP / PS1转基因小鼠的认知障碍

基本原理

淀粉样蛋白β肽（Aβ）引发一系列病理事件，包括小胶质细胞活化，氧化应激和引起炎症的神经元死亡以及阿尔茨海默氏病（AD）的典型病理变化。

目标

这项研究旨在调查球蛋白D在体内对AD的治疗作用和机制。

方法

在这项研究中，莫里斯水迷宫（MWM）分析被用来检测APP / PS1小鼠在用球囊菌素D灌胃2个月后的认知能力。通过ELISA评估Aβ40，Aβ42，IL-1β和TNF-α的水平。还通过组织学分析研究了Aβ斑块和神经炎症的生物标志物。

结果

我们建立了球蛋白D显着改善了APP / PS1转基因小鼠的认知缺陷，并降低了淀粉样斑块，Aβ40和Aβ42的水平。Bulbocodin D还降低了小胶质标记IbA1，GFAP和抗氧化酶的水平，并减少了脂质过氧化和促炎细胞因子的产生。

结论

总而言之，本研究提供了临床前证据，即口服球囊抑素D可以减轻AD病理。