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Chicoric acid supplementation prevents systemic inflammation-induced memory impairment and amyloidogenesis via inhibition of NF-κB.
- Source :
-
FASEB journal : official publication of the Federation of American Societies for Experimental Biology [FASEB J] 2017 Apr; Vol. 31 (4), pp. 1494-1507. Date of Electronic Publication: 2016 Dec 21. - Publication Year :
- 2017
-
Abstract
- Chicoric acid (CA), a natural phenolic acid extracted from chicory and the echinacea (purple coneflower) plant ( Echinacea purpurea ), has been regarded as a nutraceutical that has powerful antioxidant and antiobesity activities. We investigated the inhibitory effects of CA on systemic inflammation-induced neuroinflammation, amyloidogenesis, and cognitive impairment. C57BL/6J mice were treated with 0.05% CA in the drinking water for 45 d. The mice were then treated by intraperitoneal injection of lipopolysaccharide (LPS). It was found that CA prevented LPS-induced memory impairment and neuronal loss through behavioral tests and histological examination. Furthermore, amyloidogenesis in the CNS was detected. The results showed that CA prevented LPS-induced increases in amyloid β (1-42 specific) (Aβ <subscript>1-42</subscript> ) accumulation, levels of amyloid precursor protein, and neuronal β-secretase 1 (BACE1), as well as the equilibrium cholinergic system in mouse brain. Moreover, CA down-regulated LPS-induced glial overactivation by inhibiting the MAPK and NF-κB pathway. Consequently, CA reduced the levels of NF-κB transcriptionally regulated inflammatory mediators and cytokines such as iNOS, cyclooxygenase-2 (COX-2), IL-1β, and TNF-α in both mouse brain and BV2 microglial cells. These results demonstrated that CA alleviated memory impairment and amyloidogenesis triggered by LPS through suppressing NF-κB transcriptional pathway, suggesting that CA might be a plausible therapeutic intervention for neuroinflammation-related diseases such as Alzheimer disease.-Liu, Q., Chen, Y., Shen, C., Xiao, Y., Wang, Y., Liu, Z., Liu, X. Chicoric acid supplementation prevents systemic inflammation-induced memory impairment and amyloidogenesis via inhibition of NF-κB.<br /> (© FASEB.)
- Subjects :
- Amyloid Precursor Protein Secretases metabolism
Amyloidosis etiology
Amyloidosis prevention & control
Animals
Aspartic Acid Endopeptidases metabolism
Caffeic Acids therapeutic use
Cell Line
Cyclooxygenase 2 metabolism
Interleukin-1beta metabolism
Lipopolysaccharides toxicity
Memory Disorders etiology
Memory Disorders prevention & control
Mice
Mice, Inbred C57BL
Microglia drug effects
Microglia metabolism
Neurons drug effects
Neurons metabolism
Neuroprotective Agents therapeutic use
Nitric Oxide Synthase Type II metabolism
Succinates therapeutic use
Tumor Necrosis Factor-alpha metabolism
Amyloid beta-Peptides metabolism
Amyloidosis drug therapy
Caffeic Acids pharmacology
Memory Disorders drug therapy
NF-kappa B metabolism
Neuroprotective Agents pharmacology
Peptide Fragments metabolism
Succinates pharmacology
Subjects
Details
- Language :
- English
- ISSN :
- 1530-6860
- Volume :
- 31
- Issue :
- 4
- Database :
- MEDLINE
- Journal :
- FASEB journal : official publication of the Federation of American Societies for Experimental Biology
- Publication Type :
- Academic Journal
- Accession number :
- 28003341
- Full Text :
- https://doi.org/10.1096/fj.201601071R