Ai-She Gao, Huan Du, Qing Gao, Yi-Jing Wang, Xie-Yan Wang, Jian-Wei Liu, Bin Lu
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引用次数: 0
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.