Oridonin attenuates Aβ1-42-induced neuroinflammation and inhibits NF-κB pathway

• Published in: PloS one 2014-08, Vol.9 (8), p.e104745-e104745
• Main Authors: Wang, Sulei, Yang, Hui, Yu, Linjie, Jin, Jiali, Qian, Lai, Zhao, Hui, Xu, Yun, Zhu, Xiaolei
• Format: Article
• Language: English
• Subjects: Alzheimer Disease - drug therapy; Alzheimer Disease - metabolism; Alzheimer Disease - physiopathology; Alzheimer's disease; Amyloid beta-Peptides - drug effects; Amyloid beta-Peptides - physiology; Animals; Apoptosis; Attenuation; Base Sequence; Biology and Life Sciences; Brain; Cytokines; Dementia; Diterpenes, Kaurane - pharmacology; Diterpenes, Kaurane - therapeutic use; DNA Primers; Hippocampus - drug effects; Hippocampus - metabolism; Hippocampus - physiopathology; Hospitals; Inflammation; Inflammation - drug therapy; Medical schools; Medicine; Memory; Mice; Mice, Inbred C57BL; Neurology; NF-kappa B - metabolism; NF-κB protein; Oxidative stress; Pathogenesis; Peptide Fragments - drug effects; Peptide Fragments - physiology; Proteins; Real-Time Polymerase Chain Reaction; Rodents; Tumor necrosis factor-TNF; β-Amyloid
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0104745

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 Aβ1-42-induced AD mice. In addition, Ori inhibited the NF-κB pathway and Aβ1-42-induced apoptosis. Furthermore, Ori could attenuate memory deficits in Aβ1-42-induced AD mice. In conclusion, our study demonstrated that Ori inhibited the neuroinflammation and attenuated memory deficits induced by Aβ1-42, suggesting that Ori might be a promising candidate for AD treatment.