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Article: Berberine ameliorates β-amyloid pathology, gliosis, and cognitive impairment in an Alzheimer's disease transgenic mouse model

TitleBerberine ameliorates β-amyloid pathology, gliosis, and cognitive impairment in an Alzheimer's disease transgenic mouse model
Authors
KeywordsΒ-Amyloid
Alzheimer's Disease
Amyloid Precursor Protein
Berberine
Glycogen Synthase Kinase
Tau Phosphorylation
Tgcrnd8 Mice
Issue Date2012
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/neuaging
Citation
Neurobiology Of Aging, 2012, v. 33 n. 12, p 2903-2919 How to Cite?
AbstractThe accumulation of β-amyloid (Aβ) peptide derived from abnormal processing of amyloid precursor protein (APP) is a common pathological hallmark of Alzheimer's disease (AD) brains. In this study, we evaluated the therapeutic effect of berberine (BBR) extracted from Coptis chinensis Franch, a Chinese medicinal herb, on the neuropathology and cognitive impairment in TgCRND8 mice, a well established transgenic mouse model of AD. Two-month-old TgCRND8 mice received a low (25 mg/kg per day) or a high dose of BBR (100 mg/kg per day) by oral gavage until 6 months old. BBR treatment significantly ameliorated learning deficits, long-term spatial memory retention, as well as plaque load compared with vehicle control treatment. In addition, enzyme-linked immunosorbent assay (ELISA) measurement showed that there was a profound reduction in levels of detergent-soluble and -insoluble β-amyloid in brain homogenates of BBR-treated mice. Glycogen synthase kinase (GSK)3, a major kinase involved in APP and tau phosphorylation, was significantly inhibited by BBR treatment. We also found that BBR significantly decreased the levels of C-terminal fragments of APP and the hyperphosphorylation of APP and tau via the Akt/glycogen synthase kinase 3 signaling pathway in N2a mouse neuroblastoma cells stably expressing human Swedish mutant APP695 (N2a-SwedAPP). Our results suggest that BBR provides neuroprotective effects in TgCRND8 mice through regulating APP processing and that further investigation of the BBR for therapeutic use in treating AD is warranted. © 2012 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/149785
ISSN
2015 Impact Factor: 5.153
2015 SCImago Journal Rankings: 2.613
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorDurairajan, SSKen_US
dc.contributor.authorLiu, LFen_US
dc.contributor.authorLu, JHen_US
dc.contributor.authorChen, LLen_US
dc.contributor.authorYuan, Qen_US
dc.contributor.authorChung, SKen_US
dc.contributor.authorHuang, Len_US
dc.contributor.authorLi, XSen_US
dc.contributor.authorHuang, JDen_US
dc.contributor.authorLi, Men_US
dc.date.accessioned2012-06-26T05:58:37Z-
dc.date.available2012-06-26T05:58:37Z-
dc.date.issued2012en_US
dc.identifier.citationNeurobiology Of Aging, 2012, v. 33 n. 12, p 2903-2919en_US
dc.identifier.issn0197-4580en_US
dc.identifier.urihttp://hdl.handle.net/10722/149785-
dc.description.abstractThe accumulation of β-amyloid (Aβ) peptide derived from abnormal processing of amyloid precursor protein (APP) is a common pathological hallmark of Alzheimer's disease (AD) brains. In this study, we evaluated the therapeutic effect of berberine (BBR) extracted from Coptis chinensis Franch, a Chinese medicinal herb, on the neuropathology and cognitive impairment in TgCRND8 mice, a well established transgenic mouse model of AD. Two-month-old TgCRND8 mice received a low (25 mg/kg per day) or a high dose of BBR (100 mg/kg per day) by oral gavage until 6 months old. BBR treatment significantly ameliorated learning deficits, long-term spatial memory retention, as well as plaque load compared with vehicle control treatment. In addition, enzyme-linked immunosorbent assay (ELISA) measurement showed that there was a profound reduction in levels of detergent-soluble and -insoluble β-amyloid in brain homogenates of BBR-treated mice. Glycogen synthase kinase (GSK)3, a major kinase involved in APP and tau phosphorylation, was significantly inhibited by BBR treatment. We also found that BBR significantly decreased the levels of C-terminal fragments of APP and the hyperphosphorylation of APP and tau via the Akt/glycogen synthase kinase 3 signaling pathway in N2a mouse neuroblastoma cells stably expressing human Swedish mutant APP695 (N2a-SwedAPP). Our results suggest that BBR provides neuroprotective effects in TgCRND8 mice through regulating APP processing and that further investigation of the BBR for therapeutic use in treating AD is warranted. © 2012 Elsevier Inc. All rights reserved.en_US
dc.languageengen_US
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/neuagingen_US
dc.relation.ispartofNeurobiology of Agingen_US
dc.subjectΒ-Amyloiden_US
dc.subjectAlzheimer's Diseaseen_US
dc.subjectAmyloid Precursor Proteinen_US
dc.subjectBerberineen_US
dc.subjectGlycogen Synthase Kinaseen_US
dc.subjectTau Phosphorylationen_US
dc.subjectTgcrnd8 Miceen_US
dc.titleBerberine ameliorates β-amyloid pathology, gliosis, and cognitive impairment in an Alzheimer's disease transgenic mouse modelen_US
dc.typeArticleen_US
dc.identifier.emailChung, SK:skchung@hkucc.hku.hken_US
dc.identifier.authorityChung, SK=rp00381en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.neurobiolaging.2012.02.016en_US
dc.identifier.pmid22459600-
dc.identifier.scopuseid_2-s2.0-84866744899en_US
dc.identifier.hkuros199688-
dc.identifier.isiWOS:000310200000017-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridDurairajan, SSK=55120189300en_US
dc.identifier.scopusauthoridLiu, LF=55120472500en_US
dc.identifier.scopusauthoridLu, JH=55121813500en_US
dc.identifier.scopusauthoridChen, LL=55125549800en_US
dc.identifier.scopusauthoridYuan, Q=7202814773en_US
dc.identifier.scopusauthoridChung, SK=7404292976en_US
dc.identifier.scopusauthoridHuang, L=7404736600en_US
dc.identifier.scopusauthoridLi, XS=55121790200en_US
dc.identifier.scopusauthoridHuang, JD=55125558500en_US
dc.identifier.scopusauthoridLi, M=55121951600en_US
dc.identifier.citeulike11522637-

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