Zhou Li, Huang Jin-Yuan, Zhang Di, Zhao Ya-Liang
Health Management Center, Wuhan Hospital of Traditional Chinese Medicine, Wuhan, Hubei 430014, P.R. China.
Exp Ther Med. 2020 Aug;20(2):1082-1090. doi: 10.3892/etm.2020.8760. Epub 2020 May 17.
Alzheimer's disease (AD), is a severe neurodegenerative disease that currently lacks an optimally effective therapeutic agent for its management. Saikosaponin D (SSD) is a component extracted from the herb that is commonly used in Chinese medicine. Although SSD has been reported to exert neuroprotective effects, its pharmacological role in AD has not been previously elucidated. Therefore, the aim of the present study was to investigate whether SSD treatment improves the cognitive function and pathological features of 3xTg mice, a triple-transgenic mouse model of AD that displays classical pathological features of AD. The effects of SSD treatment on the behavioral, histological and physiological features of the animal were quantified. Results from the behavioral experiments on the SSD-treated 3xTg mice identified a significant reduction in memory impairment. In addition, histological staining results indicated that SSD application could preserve the morphology of neurons, reduce apoptosis and significantly inhibit amyloid-β deposition in the hippocampus of 3xTg mice. SSD treatment also decelerated the activation of microglia and astrocytes in the hippocampus of 3xTg mice, possibly via the inhibition of the NF-κB signal transduction pathway. Therefore, the present study demonstrated the protective effects of SSD against progressive neurodegeneration and identified the potential underlying pharmacological mechanism. It was speculated that SSD may serve as a possible therapeutic agent in AD treatment in the future.
阿尔茨海默病(AD)是一种严重的神经退行性疾病,目前在其治疗方面缺乏最佳有效的治疗药物。柴胡皂苷D(SSD)是从一种常用于中药的草药中提取的成分。尽管已有报道称SSD具有神经保护作用,但其在AD中的药理作用此前尚未阐明。因此,本研究的目的是探讨SSD治疗是否能改善3xTg小鼠的认知功能和病理特征,3xTg小鼠是一种显示AD经典病理特征的AD三联转基因小鼠模型。对SSD治疗对动物行为、组织学和生理学特征的影响进行了量化。对接受SSD治疗的3xTg小鼠进行的行为实验结果表明,记忆障碍显著减轻。此外,组织学染色结果表明,应用SSD可以保留神经元的形态,减少细胞凋亡,并显著抑制3xTg小鼠海马体中淀粉样β蛋白的沉积。SSD治疗还可能通过抑制NF-κB信号转导通路,减缓3xTg小鼠海马体中微胶质细胞和星形胶质细胞的激活。因此,本研究证明了SSD对进行性神经退行性变的保护作用,并确定了潜在的药理机制。推测SSD未来可能成为AD治疗的一种潜在治疗药物。