Tong Luo Jiu Nao, a Chinese Medicine Formula, Reduces Inflammatory Stress in a Mouse Model of Alzheimer's Disease.

Ai-She Gao, Huan Du, Qing Gao, Yi-Jing Wang, Xie-Yan Wang, Jian-Wei Liu, Bin Lu
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Abstract

Aim: The aim of this study is to extend the molecular mechanism of Tong Luo Jiu Nao (TLJN) for Alzheimer's disease (AD), which is a modern Chinese formula that has been used to treat AD.

Methods: The senescence-accelerated mouse prone 8 strain (SAMP8) is one of the most appropriate models to study the mechanism that underlies AD. The levels of plasma amyloid β (Aβ) and the Aβ deposits were measured using enzyme-linked immunosorbent assay and immunohistochemistry. Immunoblotting was used to observe the effect of TLJN on inflammatory mediator expression in an senescence-accelerated mouse model of AD.

Results: Our data showed that the TLJN-treated groups exhibited a reduction in plasma Aβ levels and reduced Aβ expression. Moreover, TLJN effectively attenuated Aβ-induced activation of extracellular signal-regulated kinase and c-Jun N-terminal kinases and blocked changes in inflammatory mediator expression.

Conclusion: These data suggest that TLJN might have protective effects and could potentially act to attenuate inflammatory stress in the pathogenesis of AD.

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中药配方通络九窍能减轻阿尔茨海默病小鼠模型的炎症应激反应
目的:本研究旨在扩展通络九窍(TLJN)治疗阿尔茨海默病(AD)的分子机制:方法:衰老加速小鼠易感8株(SAMP8)是研究AD发病机制的最合适模型之一。采用酶联免疫吸附试验和免疫组织化学方法测定血浆淀粉样β(Aβ)和Aβ沉积物的水平。免疫印迹法用于观察 TLJN 对衰老加速 AD 小鼠模型中炎性介质表达的影响:结果:我们的数据显示,TLJN处理组的血浆Aβ水平降低,Aβ表达减少。此外,TLJN 能有效减轻 Aβ 诱导的细胞外信号调节激酶和 c-Jun N 端激酶的激活,并阻止炎症介质表达的变化:这些数据表明,TLJN可能具有保护作用,并有可能在AD的发病机制中起到减轻炎症压力的作用。
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