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Cognitive improvement effects of momordica charantia in amyloid beta-induced alzheimer’s disease mouse model

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dc.contributor.authorSin, S.M.-
dc.contributor.authorKim, J.H.-
dc.contributor.authorCho, E.J.-
dc.contributor.authorKim, H.Y.-
dc.date.accessioned2022-12-26T11:46:24Z-
dc.date.available2022-12-26T11:46:24Z-
dc.date.issued2021-
dc.identifier.issn1976-0442-
dc.identifier.issn2234-7941-
dc.identifier.urihttps://scholarworks.gnu.ac.kr/handle/sw.gnu/5538-
dc.description.abstractAccumulation of amyloid beta (Aβ) and oxidative stress are the most common reason of Alzheimer’s disease (AD). In the present study, we investigated the cognitive improvement effects of butanol (BuOH) fraction from Momordica charantia in Aβ25-35-induced AD mouse model. To develop an AD mouse model, mice were received injection of Aβ25-35, and then orally administered BuOH fraction from M. charantia at doses of 100 and 200 mg/kg/day during 14 days. In the T-maze and novel object recognition test, administration of BuOH fraction from M. charantia at doses of 100 and 200 mg/kg/day improved spatial ability and novel object recognition by increased explorations of novel route and new object. In addition, BuOH fraction of M. charantia-administered groups improved learning and memory abilities by decreased time to reach hidden platform in Morris water maze test. Oral administration of BuOH fraction from M. charantia significantly inhibited lipid peroxidation and nitric oxide levels in the brain, liver, and kidney compared with Aβ25-35-induced control group. These results indicated that BuOH fraction of M. charantia improved Aβ25-35-induced cognitive impairment by attenuating oxidative stress. Therefore, M. charantia could be useful for protection from Aβ25-35-induced cognitive impairment. ? The Korean Society for Applied Biological Chemistry 2021.-
dc.format.extent9-
dc.language한국어-
dc.language.isoKOR-
dc.publisherKorean Society for Applied Biological Chemistry-
dc.titleCognitive improvement effects of momordica charantia in amyloid beta-induced alzheimer’s disease mouse model-
dc.typeArticle-
dc.publisher.location대한민국-
dc.identifier.doi10.3839/jabc.2021.041-
dc.identifier.scopusid2-s2.0-85116257636-
dc.identifier.bibliographicCitationJournal of Applied Biological Chemistry, v.64, no.3, pp 299 - 307-
dc.citation.titleJournal of Applied Biological Chemistry-
dc.citation.volume64-
dc.citation.number3-
dc.citation.startPage299-
dc.citation.endPage307-
dc.type.docTypeArticle-
dc.identifier.kciidART002756447-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscopus-
dc.description.journalRegisteredClasskci-
dc.subject.keywordAuthorAlzheimer’s disease-
dc.subject.keywordAuthorAmyloid beta-
dc.subject.keywordAuthorCognition-
dc.subject.keywordAuthorMomordica charantia-
dc.subject.keywordAuthorOxidative stress-
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