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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Alzheimer Disease / drug therapy*
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Alzheimer Disease / metabolism
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Alzheimer Disease / physiopathology
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Amyloid beta-Peptides / drug effects*
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Amyloid beta-Peptides / physiology
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Animals
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Base Sequence
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DNA Primers
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Diterpenes, Kaurane / pharmacology*
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Diterpenes, Kaurane / therapeutic use
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Hippocampus / drug effects
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Hippocampus / metabolism
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Hippocampus / physiopathology
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Inflammation / drug therapy*
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Mice
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Mice, Inbred C57BL
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NF-kappa B / metabolism*
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Peptide Fragments / drug effects*
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Peptide Fragments / physiology
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Real-Time Polymerase Chain Reaction
Substances
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Amyloid beta-Peptides
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DNA Primers
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Diterpenes, Kaurane
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NF-kappa B
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Peptide Fragments
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amyloid beta-protein (1-42)
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oridonin
Grants and funding
This study was supported by the National Nature Science Foundation of China (81200839, 81230026, and 81171085), the Natural Science Foundation (BL2012013) and the Bureau of Health (LJ201101) of the Jiangsu Province of China. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.