Rhinacanthin C Alleviates Amyloid-β Fibrils’ Toxicity on Neurons and Attenuates Neuroinflammation Triggered by LPS, Amyloid-β, and Interferon-γ in Glial Cells
Joint Authors
Chuang, Kai-An
Li, Ming-Han
Lin, Ni-Hsuan
Chang, Chih-Hsuan
Takahashi, Tomoya
Perng, Ming-Der
Wen, Shu-Fang
Lu, I-Huang
Pan, I-Horng
Source
Oxidative Medicine and Cellular Longevity
Issue
Vol. 2017, Issue 2017 (31 Dec. 2017), pp.1-18, 18 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2017-10-18
Country of Publication
Egypt
No. of Pages
18
Main Subjects
Abstract EN
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.
American Psychological Association (APA)
Chuang, Kai-An& Li, Ming-Han& Lin, Ni-Hsuan& Chang, Chih-Hsuan& Lu, I-Huang& Pan, I-Horng…[et al.]. 2017. Rhinacanthin C Alleviates Amyloid-β Fibrils’ Toxicity on Neurons and Attenuates Neuroinflammation Triggered by LPS, Amyloid-β, and Interferon-γ in Glial Cells. Oxidative Medicine and Cellular Longevity،Vol. 2017, no. 2017, pp.1-18.
https://search.emarefa.net/detail/BIM-1194960
Modern Language Association (MLA)
Chuang, Kai-An…[et al.]. Rhinacanthin C Alleviates Amyloid-β Fibrils’ Toxicity on Neurons and Attenuates Neuroinflammation Triggered by LPS, Amyloid-β, and Interferon-γ in Glial Cells. Oxidative Medicine and Cellular Longevity No. 2017 (2017), pp.1-18.
https://search.emarefa.net/detail/BIM-1194960
American Medical Association (AMA)
Chuang, Kai-An& Li, Ming-Han& Lin, Ni-Hsuan& Chang, Chih-Hsuan& Lu, I-Huang& Pan, I-Horng…[et al.]. Rhinacanthin C Alleviates Amyloid-β Fibrils’ Toxicity on Neurons and Attenuates Neuroinflammation Triggered by LPS, Amyloid-β, and Interferon-γ in Glial Cells. Oxidative Medicine and Cellular Longevity. 2017. Vol. 2017, no. 2017, pp.1-18.
https://search.emarefa.net/detail/BIM-1194960
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1194960