Alginate-Derived Oligosaccharide Inhibits Neuroinflammation and Promotes Microglial Phagocytosis of β-Amyloid

Alginate from marine brown algae has been widely applied in biotechnology. In this work, the effects of alginate-derived oligosaccharide (AdO) on lipopolysaccharide (LPS)/β-amyloid (Aβ)-induced neuroinflammation and microglial phagocytosis of Aβ were studied. We found that pretreatment of BV2 microg...

Full description

Saved in:
Bibliographic Details
Published in:Marine drugs 2015-09, Vol.13 (9), p.5828-5846
Main Authors: Zhou, Rui, Shi, Xu-Yang, Bi, De-Cheng, Fang, Wei-Shan, Wei, Gao-Bin, Xu, Xu
Format: Article
Language:English
Subjects:
alginate
Alginates - chemistry
Amyloid beta-Peptides - metabolism
Amyloid beta-Peptides - toxicity
Animals
Cell Line
Cell Survival - drug effects
Cytokines - genetics
Cytokines - metabolism
Dinoprostone - metabolism
Gene Expression Regulation, Enzymologic - drug effects
Glucuronic Acid - chemistry
Hexuronic Acids - chemistry
Inflammation - drug therapy
Lipopolysaccharides - toxicity
Marine
microglia
Microglia - drug effects
Microglia - physiology
neuroinflammation
Nitric Oxide - metabolism
Oligosaccharides - chemistry
Oligosaccharides - pharmacology
phagocytosis
Phagocytosis - drug effects
toll-like receptor 4
β-amyloid
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Alginate from marine brown algae has been widely applied in biotechnology. In this work, the effects of alginate-derived oligosaccharide (AdO) on lipopolysaccharide (LPS)/β-amyloid (Aβ)-induced neuroinflammation and microglial phagocytosis of Aβ were studied. We found that pretreatment of BV2 microglia with AdO prior to LPS/Aβ stimulation led to a significant inhibition of production of nitric oxide (NO) and prostaglandin E₂ (PGE₂), expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) and secretion of proinflammatory cytokines. We further demonstrated that AdO remarkably attenuated the LPS-activated overexpression of toll-like receptor 4 (TLR4) and nuclear factor (NF)-κB in BV2 cells. In addition to the impressive inhibitory effect on neuroinflammation, we also found that AdO promoted the phagocytosis of Aβ through its interaction with TLR4 in microglia. Our results suggested that AdO exerted the inhibitory effect on neuroinflammation and the promotion effect on microglial phagocytosis, indicating its potential as a nutraceutical or therapeutic agent for neurodegenerative diseases, particularly Alzheimer's disease (AD).
ISSN:1660-3397
1660-3397
DOI:10.3390/md13095828