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

Author:

Chuang Kai-An1,Li Ming-Han1,Lin Ni-Hsuan2,Chang Chih-Hsuan1,Lu I-Huang1ORCID,Pan I-Hong1,Takahashi Tomoya3,Perng Ming-Der2ORCID,Wen Shu-Fang1ORCID

Affiliation:

1. Biomedical Technology and Device Research Laboratories, Industrial Technology Research Institute, 321 Kuang Fu 2nd Road, Hsinchu 30011, Taiwan

2. Institute of Molecular Medicine, College of Life Sciences, National Tsing Hua University, 101 Kuang Fu 2nd Road, Hsinchu 30013, Taiwan

3. ARSOA Research & Development Center, AOB Keioh Group Corp., 2961 Kobuchisawa-cho, Hokuto, Yamanashi 408-8522, Japan

Abstract

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.

Funder

Ministry of Science and Technology of the People’s Republic of China

Publisher

Hindawi Limited

Subject

Cell Biology,Ageing,General Medicine,Biochemistry

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