Oridonin attenuates Aβ1-42-induced neuroinflammation and inhibits NF-κB pathway.
basic_science · Level V
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- Record sourced from PubMed, PMID 25121593.
- Also identified by DOI 10.1371/journal.pone.0104745 and PMC identifier 4133239.
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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.
Medical subject headings
- Alzheimer Disease
- Amyloid beta-Peptides
- Diterpenes, Kaurane
- Inflammation
- NF-kappa B
- Peptide Fragments