Oridonin Attenuates Aβ1–42-Induced Neuroinflammation and Inhibits NF-κB Pathway |
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Authors: | Sulei Wang Hui Yang Linjie Yu Jiali Jin Lai Qian Hui Zhao Yun Xu Xiaolei Zhu |
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Institution: | 1. Department of Neurology, Nanjing Drum Tower Hospital Clinical College of Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing, P. R. China.; 2. Department of Neurology, Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing, P. R. China.; Massachusetts General Hospital, United States of America, |
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Abstract: | 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. |
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