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Gallic acid, a histone acetyltransferase inhibitor, suppresses β-amyloid neurotoxicity by inhibiting microglial-mediated neuroinflammation

Authors
 Mi-Jeong Kim  ;  Ah-Reum Seong  ;  Jung-Yoon Yoo  ;  Cheng-Hao Jin  ;  Yoo-Hyun Lee  ;  Young Jun Kim  ;  Jeongmin Lee  ;  Woo Jin Jun  ;  Ho-Geun Yoon 
Citation
 MOLECULAR NUTRITION & FOOD RESEARCH, Vol.55(12) : 1798-1808, 2011 
Journal Title
MOLECULAR NUTRITION & FOOD RESEARCH
ISSN
 1613-4125 
Issue Date
2011
MeSH
Amyloid beta-Peptides/toxicity* ; Animals ; Blotting, Western ; Cell Survival/drug effects ; Coculture Techniques ; Cytokines/biosynthesis ; Cytokines/drug effects ; Cytokines/genetics ; Down-Regulation ; Enzyme Inhibitors/pharmacology* ; Gallic Acid/pharmacology* ; Histone Acetyltransferases/antagonists & inhibitors ; Histone Acetyltransferases/metabolism ; Inflammation/drug therapy ; Inflammation/pathology* ; Male ; Mice ; Mice, Inbred ICR ; Microglia/cytology ; Microglia/drug effects* ; NF-kappa B/antagonists & inhibitors ; NF-kappa B/genetics ; NF-kappa B/metabolism ; Neurons/cytology ; Neurons/drug effects ; Neurotoxicity Syndromes/pathology* ; Real-Time Polymerase Chain Reaction
Keywords
Alzheimer disease ; Gallic acid ; Histone acetyltransferase inhibitor ; Microglia ; Neuroinflammation
Abstract
SCOPE: We examined the biological effect of gallic acid (GA) as a nuclear factor (NF)-κB acetyltransferase inhibitor on microglial-mediated β-amyloid neurotoxicity and restorative effects on the Aβ-induced cognitive dysfunction.

METHODS AND RESULTS: The protective effects of GA on the survival of neuronal cells were assessed with an MTT assay and a co-culture system. For the co-culture experiments, both BV-2 and primary microglia cells were treated with GA prior to Aβ stimulation, and conditioned media were transferred to Neuro-2A cells. The mRNA and protein levels of inflammatory cytokines in both microglia and Neuro-2A cells were assessed with real-time polymerase chain reaction and western blotting. Inhibition of nuclear factor kappa B (NF-κB) acetylation with GA treatment resulted in reduced cytokine production in microglia cells and protection of neuronal cells from Aβ-induced neurotoxicity. Furthermore, we observed a restorative effect of GA on Aβ-induced cognitive dysfunction in mice with Y-maze and passive avoidance tests. Finally, we found that GA treatment efficiently blocked neuronal cell death by downregulating the expression of cytokines and the in vivo levels of NF-κB acetylation.

CONCLUSION: These results suggest that selective inhibition of NF-κB acetylation by the histone acetyltransferase inhibitor GA is a possible therapeutic approach for alleviating the inflammatory progression of Alzheimer disease
Full Text
http://onlinelibrary.wiley.com/doi/10.1002/mnfr.201100262/abstract
DOI
10.1002/mnfr.201100262
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Biochemistry and Molecular Biology (생화학-분자생물학교실) > 1. Journal Papers
Yonsei Authors
Kim, Mi Jeong(김미정) ORCID logo https://orcid.org/0000-0002-0758-7145
Yoo, Jung Yoon(유정윤) ORCID logo https://orcid.org/0000-0001-9366-3863
Yoon, Ho Geun(윤호근) ORCID logo https://orcid.org/0000-0003-2718-3372
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/94647
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