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Oridonin Attenuates Aβ(1–42)-Induced Neuroinflammation and Inhibits NF-κB Pathway

Neuroinflammation induced by beta-amyloid (Aβ) plays a critical role in the pathogenesis of Alzheimer’s disease (AD), and inhibiting Aβ-induced neuroinflammation serves as a potential strategy for the treatment of AD. Oridonin (Ori), a compound of Rabdosia rubescens, has been shown to exert anti-inf...

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Detalles Bibliográficos
Autores principales: Wang, Sulei, Yang, Hui, Yu, Linjie, Jin, Jiali, Qian, Lai, Zhao, Hui, Xu, Yun, Zhu, Xiaolei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4133239/
https://www.ncbi.nlm.nih.gov/pubmed/25121593
http://dx.doi.org/10.1371/journal.pone.0104745
Descripción
Sumario:Neuroinflammation induced by beta-amyloid (Aβ) plays a critical role in the pathogenesis of Alzheimer’s disease (AD), and inhibiting Aβ-induced neuroinflammation serves as a potential strategy for the treatment of AD. Oridonin (Ori), a compound of Rabdosia rubescens, has been shown to exert anti-inflammatory effects. In this study, we demonstrated that Ori inhibited glial activation and decreased the release of inflammatory cytokines in the hippocampus of Aβ(1–42)-induced AD mice. In addition, Ori inhibited the NF-κB pathway and Aβ(1–42)-induced apoptosis. Furthermore, Ori could attenuate memory deficits in Aβ(1–42)-induced AD mice. In conclusion, our study demonstrated that Ori inhibited the neuroinflammation and attenuated memory deficits induced by Aβ(1–42), suggesting that Ori might be a promising candidate for AD treatment.