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Cinnamomum loureirii Extract Inhibits Acetylcholinesterase Activity and Ameliorates Trimethyltin-Induced Cognitive Dysfunction in Mice

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dc.contributor.authorKim, Cho Rong-
dc.contributor.authorChoi, Soo Jung-
dc.contributor.authorKwon, Yoon Kyung-
dc.contributor.authorKim, Jae Kyeom-
dc.contributor.authorKim, Youn-Jung-
dc.contributor.authorPark, Gwi Gun-
dc.contributor.authorShin, Dong-Hoon-
dc.date.available2020-02-28T01:43:23Z-
dc.date.created2020-02-06-
dc.date.issued2016-07-
dc.identifier.issn0918-6158-
dc.identifier.urihttps://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/8133-
dc.description.abstractThe pathogenesis of Alzheimer's disease (AD) has been linked to the deficiency of neurotransmitter acetylcholine (ACh) in the brain, and the main treatment strategy for improving AD symptoms is the inhibition of acetylcholinesterase (AChE) activity. In the present study, we aimed to identify potent AChE inhibitors from Cinnamomum loureirii extract via bioassay-guided fractionation. We demonstrated that the most potent AChE inhibitor present in the C. loureirii extract was 2,4-bis(1,1-dimethylethyl)phenol. To confirm the antiamnesic effects of the ethanol extract of C. loureirii, mice were intraperitoneally injected with the neurotoxin trimethyltin (2.5mg/kg) to induce cognitive dysfunction, and performance in the Y-maze and passive avoidance tests was assessed. Treatment with C. loureirii extract significantly improved performance in both behavioral tests, suggesting that this extract may be neuroprotective and therefore beneficial in preventing or ameliorating the degenerative processes of AD, potentially by restoring cholinergic function.-
dc.language영어-
dc.language.isoen-
dc.publisherPHARMACEUTICAL SOC JAPAN-
dc.relation.isPartOfBIOLOGICAL & PHARMACEUTICAL BULLETIN-
dc.subjectALZHEIMERS-DISEASE-
dc.subjectCHOLINESTERASE-INHIBITORS-
dc.subject2,4-DI-TERT-BUTYLPHENOL-
dc.subjectDERIVATIVES-
dc.titleCinnamomum loureirii Extract Inhibits Acetylcholinesterase Activity and Ameliorates Trimethyltin-Induced Cognitive Dysfunction in Mice-
dc.typeArticle-
dc.type.rimsART-
dc.description.journalClass1-
dc.identifier.wosid000378974400008-
dc.identifier.doi10.1248/bpb.b16-00045-
dc.identifier.bibliographicCitationBIOLOGICAL & PHARMACEUTICAL BULLETIN, v.39, no.7, pp.1130 - 1136-
dc.identifier.scopusid2-s2.0-84978035518-
dc.citation.endPage1136-
dc.citation.startPage1130-
dc.citation.titleBIOLOGICAL & PHARMACEUTICAL BULLETIN-
dc.citation.volume39-
dc.citation.number7-
dc.contributor.affiliatedAuthorPark, Gwi Gun-
dc.type.docTypeArticle-
dc.subject.keywordAuthorAlzheimer&apos-
dc.subject.keywordAuthors disease-
dc.subject.keywordAuthorCinnamomum loureirii-
dc.subject.keywordAuthoracetylcholine-
dc.subject.keywordAuthoracetylcholinesterase inhibitor-
dc.subject.keywordPlusALZHEIMERS-DISEASE-
dc.subject.keywordPlusCHOLINESTERASE-INHIBITORS-
dc.subject.keywordPlus2,4-DI-TERT-BUTYLPHENOL-
dc.subject.keywordPlusDERIVATIVES-
dc.relation.journalResearchAreaPharmacology & Pharmacy-
dc.relation.journalWebOfScienceCategoryPharmacology & Pharmacy-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
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