Geniposide Attenuates Oligomeric Aβ<sub>1-42</sub>-Induced Inflammatory Response by Targeting RAGE-Dependent Signaling in BV2 Cells

ISSN: 1875-5828 (Online)
ISSN: 1567-2050 (Print)


Volume 11, 10 Issues, 2014


Download PDF Flyer




Current Alzheimer Research

Aims & ScopeAbstracted/Indexed in

Ranking and Category:
  • 38th of 194 in Clinical Neurology
  • 80th of 251 in Neurosciences

Submit Abstracts Online Submit Manuscripts Online

Editor-in-Chief:
Prof. Debomoy K. Lahiri
Department of Psychiatry, Indiana University School of Medicine
Neuroscience Research Center
Indianapolis, IN 46202
USA


View Full Editorial Board

Subscribe Purchase Articles Order Reprints

Current: 3.796
5 - Year: 3.998

Geniposide Attenuates Oligomeric Aβ1-42-Induced Inflammatory Response by Targeting RAGE-Dependent Signaling in BV2 Cells

Author(s): Cui Lv, Lei Wang, Xiaoli Liu, Xiao Cong, Shirley ShiDu Yan, Yongyan Wang and Wensheng Zhang

Affiliation: C Building, Beijing Normal University Science Park, No. 12, Xueyuan Southern Street, Haidian District, Beijing, P.R.China, 100088.

Abstract

The neuroinflammation induced by amyloid-β (Aβ ) is one of the key events in Alzheimer’s disease (AD) progress in which microglia are the main cells involved. Receptor for advanced glycation end products (RAGE) mediates and enhances A β-induced microglial activation and leads to induction of proinflammatory mediators, such as tumor necrosis factor- α (TNF-α ) and interleukin-1β (IL-1 β). Geniposide, a pharmacologically active component purified from gardenia fruit, exhibits a broad spectrum anti-inflammatory effect as well as neurotrophic and neuroprotective properties. However, the effects of geniposide on A β-mediated microglial pathways have not been fully discovered. Here, we demonstrate that geniposide treatment significantly blocks Aβ -induced RAGE-dependent signaling (activation of ERK and NF-κ B) along with the production of TNF- α and IL-1β in cultured BV2 microglia cells. Notably, based on the data from coimmunoprecipitation assay, we infer that geniposide exerts protective effects on A β-induced inflammatroy response through blocking A β binding to RAGE and suppressing the RAGE-mediated signaling pathway. Taken together, these findings indicate that geniposide is a potent suppressor of neuroflammation through inhibiting RAGE-dependent signaling pathway. Thus, geniposide may be a potential therapeutic agent for the treatment of neuroinflammation that is involved in neurological diseases such as AD.

Keywords: Alzheimer’s disease, geniposide, inflammatory responses, oligomeric Aβ 1-42, RAGE, RAGE-dependent signaling pathway.

Purchase Online Rights and Permissions

  
  



Article Details

Volume: 11
Issue Number: 5
First Page: 430
Last Page: 440
Page Count: 11
DOI: 10.2174/1567205011666140514111204
Advertisement

Related Journals




Webmaster Contact: urooj@benthamscience.org Copyright © 2014 Bentham Science