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

DC Field Value Language
dc.contributor.author유정윤-
dc.contributor.author윤호근-
dc.contributor.author김미정-
dc.date.accessioned2014-12-20T17:27:44Z-
dc.date.available2014-12-20T17:27:44Z-
dc.date.issued2011-
dc.identifier.issn1613-4125-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/94647-
dc.description.abstractSCOPE: 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-
dc.description.statementOfResponsibilityopen-
dc.relation.isPartOfMOLECULAR NUTRITION & FOOD RESEARCH-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAmyloid beta-Peptides/toxicity*-
dc.subject.MESHAnimals-
dc.subject.MESHBlotting, Western-
dc.subject.MESHCell Survival/drug effects-
dc.subject.MESHCoculture Techniques-
dc.subject.MESHCytokines/biosynthesis-
dc.subject.MESHCytokines/drug effects-
dc.subject.MESHCytokines/genetics-
dc.subject.MESHDown-Regulation-
dc.subject.MESHEnzyme Inhibitors/pharmacology*-
dc.subject.MESHGallic Acid/pharmacology*-
dc.subject.MESHHistone Acetyltransferases/antagonists & inhibitors-
dc.subject.MESHHistone Acetyltransferases/metabolism-
dc.subject.MESHInflammation/drug therapy-
dc.subject.MESHInflammation/pathology*-
dc.subject.MESHMale-
dc.subject.MESHMice-
dc.subject.MESHMice, Inbred ICR-
dc.subject.MESHMicroglia/cytology-
dc.subject.MESHMicroglia/drug effects*-
dc.subject.MESHNF-kappa B/antagonists & inhibitors-
dc.subject.MESHNF-kappa B/genetics-
dc.subject.MESHNF-kappa B/metabolism-
dc.subject.MESHNeurons/cytology-
dc.subject.MESHNeurons/drug effects-
dc.subject.MESHNeurotoxicity Syndromes/pathology*-
dc.subject.MESHReal-Time Polymerase Chain Reaction-
dc.titleGallic acid, a histone acetyltransferase inhibitor, suppresses β-amyloid neurotoxicity by inhibiting microglial-mediated neuroinflammation-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Biochemistry & Molecular Biology (생화학,분자생물학)-
dc.contributor.googleauthorMi-Jeong Kim-
dc.contributor.googleauthorAh-Reum Seong-
dc.contributor.googleauthorJung-Yoon Yoo-
dc.contributor.googleauthorCheng-Hao Jin-
dc.contributor.googleauthorYoo-Hyun Lee-
dc.contributor.googleauthorYoung Jun Kim-
dc.contributor.googleauthorJeongmin Lee-
dc.contributor.googleauthorWoo Jin Jun-
dc.contributor.googleauthorHo-Geun Yoon-
dc.identifier.doi10.1002/mnfr.201100262-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA02625-
dc.contributor.localIdA02502-
dc.relation.journalcodeJ02264-
dc.identifier.eissn1613-4133-
dc.identifier.pmid22038937-
dc.identifier.urlhttp://onlinelibrary.wiley.com/doi/10.1002/mnfr.201100262/abstract-
dc.subject.keywordAlzheimer disease-
dc.subject.keywordGallic acid-
dc.subject.keywordHistone acetyltransferase inhibitor-
dc.subject.keywordMicroglia-
dc.subject.keywordNeuroinflammation-
dc.contributor.alternativeNameYoo, Jung Yoon-
dc.contributor.alternativeNameYoon, Ho Geun-
dc.contributor.affiliatedAuthorYoon, Ho Geun-
dc.contributor.affiliatedAuthorYoo, Jung Yoon-
dc.contributor.affiliatedAuthor유정윤-
dc.rights.accessRightsnot free-
dc.citation.volume55-
dc.citation.number12-
dc.citation.startPage1798-
dc.citation.endPage1808-
dc.identifier.bibliographicCitationMOLECULAR NUTRITION & FOOD RESEARCH, Vol.55(12) : 1798-1808, 2011-
dc.identifier.rimsid27474-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Biochemistry and Molecular Biology (생화학-분자생물학교실) > 1. Journal Papers

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