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Oxidative Medicine and Cellular Longevity
Volume 2017 (2017), Article ID 5414297, 18 pages
Research Article

Rhinacanthin C Alleviates Amyloid-β Fibrils’ Toxicity on Neurons and Attenuates Neuroinflammation Triggered by LPS, Amyloid-β, and Interferon-γ in Glial Cells

1Biomedical Technology and Device Research Laboratories, Industrial Technology Research Institute, 321 Kuang Fu 2nd Road, Hsinchu 30011, Taiwan
2Institute of Molecular Medicine, College of Life Sciences, National Tsing Hua University, 101 Kuang Fu 2nd Road, Hsinchu 30013, Taiwan
3ARSOA Research & Development Center, AOB Keioh Group Corp., 2961 Kobuchisawa-cho, Hokuto, Yamanashi 408-8522, Japan

Correspondence should be addressed to Ming-Der Perng and Shu-Fang Wen

Received 21 May 2017; Revised 1 August 2017; Accepted 22 August 2017; Published 18 October 2017

Academic Editor: Amira Zarrouk

Copyright © 2017 Kai-An Chuang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Neuroinflammation plays a central role in the pathophysiology of Alzheimer’s disease (AD). Compounds that suppress neuroinflammation have been identified as potential therapeutic targets for AD. Rhinacanthin C (RC), a naphthoquinone ester found in Rhinacanthus nasutus Kurz (Acanthaceae), is currently proposed as an effective molecule against inflammation. However, the exact role of RC on neuroinflammation remains to be elucidated. In the present study, we investigated RC effect on modulating lipopolysaccharides (LPS), amyloid-β peptide (Aβ), or interferon-γ- (IFN-γ-) evoked pathological events in neurons and glia. Our findings demonstrated that RC prevented Aβ-induced toxicity in rat hippocampal neurons and attenuated LPS-activated nitric oxide (NO) production, inducible nitric oxide synthase (iNOS) expression, and NF-κB signaling in rat glia. Likewise, RC suppressed LPS-induced neuroinflammation by reducing NO production and iNOS, IL-1β, CCL-2, and CCL-5 mRNA levels in rat microglia. Further studies using BV-2 microglia revealed that RC inhibited LPS-, Aβ-, and IFN-γ-stimulated IL-6 and TNF-α secretion. Of note, NF-κB and ERK activation was abrogated by RC in BV-2 cell response to Aβ or IFN-γ. Moreover, RC protected neurons from Aβ-stimulated microglial conditioned media-dependent toxicity. Collectively, these data highlight the beneficial effects of RC on neuroprotection and support the therapeutic implications of RC to neuroinflammation-mediated conditions.