Cargando…

Naoling decoction restores cognitive function by inhibiting the neuroinflammatory network in a rat model of Alzheimer’s disease

Neuroinflammation is central to the pathogenesis of Alzheimer's disease (AD). We previously showed that Naoling decoction (NLD), a traditional Chinese medicine, was effective against AD, acting by inhibiting expression of IL-1β and IL-6. In the present study, we generated the rat model of AD by...

Descripción completa

Detalles Bibliográficos
Autores principales: Xia, Zian, Peng, Weijun, Cheng, Shunhua, Zhong, Bingwu, Sheng, Chenxia, Zhang, Chunhu, Gong, Wei, Cheng, Shuai, Li, Jun, Wang, Zhe
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5522095/
https://www.ncbi.nlm.nih.gov/pubmed/28487495
http://dx.doi.org/10.18632/oncotarget.17337
Descripción
Sumario:Neuroinflammation is central to the pathogenesis of Alzheimer's disease (AD). We previously showed that Naoling decoction (NLD), a traditional Chinese medicine, was effective against AD, acting by inhibiting expression of IL-1β and IL-6. In the present study, we generated the rat model of AD by injecting Aβ(1–42) peptide intracerebroventricularly and evaluated the dose-dependent effects of NLD treatment. The NLD-treated rats exhibited significant improvements in cognitive function as evaluated by the Morris water maze test. Golgi-Cox staining revealed that NLD treatment dose-dependently increased dendritic spines in the CA1 region, which were diminished in vehicle-treated rats. Further, NLD treatment normalized hippocampal Chromogranin A levels, which were elevated by Aβ(1-42) induction. NLD also attenuated activation of microglia and astrocytes induced by Aβ(1-42). Subsequently, NLD dose-dependently reduced levels TNF-α, IL-1β and IL-6 by inhibiting the NF-κB signaling pathway and the ASC-dependent inflammasome in the hippocampus. These findings reveal that NLD is a promising therapeutic agent that exerts inhibitory effects at multiple sites within the neuroinflammatory network induced in AD.