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      KCI등재후보

      Effects of Flavonoid Compounds on β-amyloid-peptide-induced Neuronal Death in Cultured Mouse Cortical Neurons

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      https://www.riss.kr/link?id=A104021586

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      다국어 초록 (Multilingual Abstract)

      Excessive accumulation of β-amyloid peptide (Aβ) is one of the major mechanisms responsiblefor neuronal death in Alzheimer’s disease. Flavonoids, primarily antioxidants,are a group of polyphenolic compounds synthesized in plant cells. The presentstudy aimed to identify flavonoid compounds that could inhibit Aβ-induced neuronaldeath by examining the effects of various flavonoids on the neurotoxicity of Aβ fragment25-35 (Aβ25-35) in mouse cortical cultures. Aβ25-35 induced concentration- and exposure-time-dependent neuronal death. Neuronal death induced by 20 μM Aβ25-35 wassignificantly inhibited by treatment with either Trolox or ascorbic acid. Among 10 flavonoidcompounds tested [apigenin, baicalein, catechin, epicatechin, epigallocatechingallate (EGCG), kaempferol, luteolin, myricetin, quercetin, and rutin], all except apigeninshowed strong 1,1-diphenyl-2-pycrylhydrazyl (DPPH) scavenging activity undercell-free conditions. The flavonoid compounds except apigenin at a concentration of 30μM also significantly inhibited neuronal death induced by 20 μM Aβ25-35 at the end of24 hours of exposure. Epicatechin, EGCG, luteolin, and myricetin showed more potentand persistent neuroprotective action than did the other compounds. These resultsdemonstrated that oxidative stress was involved in Aβ-induced neuronal death, andantioxidative flavonoid compounds, especially epicatechin, EGCG, luteolin, and myricetin,could inhibit neuronal death. These findings suggest that these four compoundsmay be developed as neuroprotective agents against Alzheimer’s disease.
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      Excessive accumulation of β-amyloid peptide (Aβ) is one of the major mechanisms responsiblefor neuronal death in Alzheimer’s disease. Flavonoids, primarily antioxidants,are a group of polyphenolic compounds synthesized in plant cells. The presents...

      Excessive accumulation of β-amyloid peptide (Aβ) is one of the major mechanisms responsiblefor neuronal death in Alzheimer’s disease. Flavonoids, primarily antioxidants,are a group of polyphenolic compounds synthesized in plant cells. The presentstudy aimed to identify flavonoid compounds that could inhibit Aβ-induced neuronaldeath by examining the effects of various flavonoids on the neurotoxicity of Aβ fragment25-35 (Aβ25-35) in mouse cortical cultures. Aβ25-35 induced concentration- and exposure-time-dependent neuronal death. Neuronal death induced by 20 μM Aβ25-35 wassignificantly inhibited by treatment with either Trolox or ascorbic acid. Among 10 flavonoidcompounds tested [apigenin, baicalein, catechin, epicatechin, epigallocatechingallate (EGCG), kaempferol, luteolin, myricetin, quercetin, and rutin], all except apigeninshowed strong 1,1-diphenyl-2-pycrylhydrazyl (DPPH) scavenging activity undercell-free conditions. The flavonoid compounds except apigenin at a concentration of 30μM also significantly inhibited neuronal death induced by 20 μM Aβ25-35 at the end of24 hours of exposure. Epicatechin, EGCG, luteolin, and myricetin showed more potentand persistent neuroprotective action than did the other compounds. These resultsdemonstrated that oxidative stress was involved in Aβ-induced neuronal death, andantioxidative flavonoid compounds, especially epicatechin, EGCG, luteolin, and myricetin,could inhibit neuronal death. These findings suggest that these four compoundsmay be developed as neuroprotective agents against Alzheimer’s disease.

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      참고문헌 (Reference)

      1 Bruce AJ, "beta-Amyloid toxicity in organotypic hippocampal cultures: protection by EUK-8, a synthetic catalytic free radical scavenger" 93 : 2312-2316, 1996

      2 Lu MF, "Where do health benefits of flavonoids come from? Insights from flavonoid targets and their evolutionary history" 434 : 701-704, 2013

      3 Kang J, "The precursor of Alzheimer's disease amyloid A4 protein resembles a cell-surface receptor" 325 : 733-736, 1987

      4 Liu R, "The flavonoid apigenin protects brain neurovascular coupling against amyloid-β25−35-induced toxicity in mice" 24 : 85-100, 2011

      5 Oken BS, "The efficacy of Ginkgo biloba on cognitive function in Alzheimer disease" 55 : 1409-1415, 1998

      6 Bastianetto S, "The Ginkgo biloba extract (EGb 761) protects hippocampal neurons against cell death induced by beta-amyloid" 12 : 1882-1890, 2000

      7 Jones QR, "Targetbased selection of flavonoids for neurodegenerative disorders" 33 : 602-610, 2012

      8 Rice-Evans CA, "Structure-antioxidant activity relationships of flavonoids and phenolic acids" 20 : 933-956, 1996

      9 Pike CJ, "Structure-activity analyses of beta-amyloid peptides: contributions of the beta 25-35 region to aggregation and neurotoxicity" 64 : 253-265, 1995

      10 Jordán J, "Role of calpain- and interleukin-1 beta converting enzyme-like proteases in the beta-amyloid-induced death of rat hippocampal neurons in culture" 1612-1621, 1997

      1 Bruce AJ, "beta-Amyloid toxicity in organotypic hippocampal cultures: protection by EUK-8, a synthetic catalytic free radical scavenger" 93 : 2312-2316, 1996

      2 Lu MF, "Where do health benefits of flavonoids come from? Insights from flavonoid targets and their evolutionary history" 434 : 701-704, 2013

      3 Kang J, "The precursor of Alzheimer's disease amyloid A4 protein resembles a cell-surface receptor" 325 : 733-736, 1987

      4 Liu R, "The flavonoid apigenin protects brain neurovascular coupling against amyloid-β25−35-induced toxicity in mice" 24 : 85-100, 2011

      5 Oken BS, "The efficacy of Ginkgo biloba on cognitive function in Alzheimer disease" 55 : 1409-1415, 1998

      6 Bastianetto S, "The Ginkgo biloba extract (EGb 761) protects hippocampal neurons against cell death induced by beta-amyloid" 12 : 1882-1890, 2000

      7 Jones QR, "Targetbased selection of flavonoids for neurodegenerative disorders" 33 : 602-610, 2012

      8 Rice-Evans CA, "Structure-antioxidant activity relationships of flavonoids and phenolic acids" 20 : 933-956, 1996

      9 Pike CJ, "Structure-activity analyses of beta-amyloid peptides: contributions of the beta 25-35 region to aggregation and neurotoxicity" 64 : 253-265, 1995

      10 Jordán J, "Role of calpain- and interleukin-1 beta converting enzyme-like proteases in the beta-amyloid-induced death of rat hippocampal neurons in culture" 1612-1621, 1997

      11 Gao J, "Research progress on natural products from traditional Chinese medicine in treatment of Alzheimer's disease" 7 : 46-57, 2013

      12 Koh JY, "Quantitative determination of glutamate mediated cortical neuronal injury in cell culture by lactate dehydrogenase efflux assay" 20 : 83-90, 1987

      13 Okada Y, "Protective effects of plant seed extracts against amyloid β-induced neurotoxicity in cultured hippocampal neurons" 5 : 141-147, 2013

      14 Drieu K, "Preparation and definition of Ginkgo biloba extract" 15 : 1455-1457, 1986

      15 Terry RD, "Physical basis of cognitive alterations in Alzheimer's disease:synapse loss is the major correlate of cognitive impairment" 30 : 572-580, 1991

      16 Beecher GR, "Overview of dietary flavonoids: nomenclature, occurrence and intake" 133 : 3248S-3254S, 2003

      17 Goodman Y, "Nordihydroguaiaretic acid protects hippocampal neurons against amyloid beta-peptide toxicity, and attenuates free radical and calcium accumulation" 654 : 171-176, 1994

      18 Zeng LH, "Neuroprotective effects of flavonoids extracted from licorice on kainate-induced seizure in mice through their antioxidant properties" 14 : 1004-1012, 2013

      19 Pike CJ, "Neurodegeneration induced by beta-amyloid peptides in vitro:the role of peptide assembly state" 13 : 1676-1687, 1993

      20 Fratiglioni L, "Incidence of dementia and major subtypes in Europe: A collaborative study of population-based cohorts. Neurologic Diseases in the Elderly Research Group" 54 (54): S10-S15, 2000

      21 Pike CJ, "In vitro aging of beta-amyloid protein causes peptide aggregation and neurotoxicity" 563 : 311-314, 1991

      22 Choi DW, "Glutamate neurotoxicity in cortical cell culture" 7 : 357-368, 1987

      23 Nijveldt RJ, "Flavonoids: a review of probable mechanisms of action and potential applications" 74 : 418-425, 2001

      24 Cho JG, "Flavonoids from the grains of C1/R-S transgenic rice, the transgenic Oryza sativa spp. japonica, and their radical scavenging activities" 61 : 10354-10359, 2013

      25 Pietta PG, "Flavonoids as antioxidants" 63 : 1035-1042, 2000

      26 Beking K, "Flavonoid intake and disability-adjusted life years due to Alzheimer's and related dementias: a populationbased study involving twenty-three developed countries" 13 : 1403-1409, 2010

      27 Letenneur L, "Flavonoid intake and cognitive decline over a 10-year period" 165 : 1364-1371, 2007

      28 Harnly JM, "Flavonoid content of U.S. fruits, vegetables, and nuts" 54 : 9966-9977, 2006

      29 Thilakarathna SH, "Flavonoid bioavailability and attempts for bioavailability enhancement" 5 : 3367-3387, 2013

      30 Dugas AJ Jr, "Evaluation of the total peroxyl radical-scavenging capacity of flavonoids: structure-activity relationships" 63 : 327-331, 2000

      31 Smid SD, "Dietary polyphenol-derived protection against neurotoxic β-amyloid protein: from molecular to clinical" 3 : 1242-1250, 2012

      32 Youdim KA, "Dietary flavonoids as potential neuroprotectants" 383 : 503-519, 2002

      33 Hertog MG, "Dietary antioxidant flavonoids and risk of coronary heart disease:the Zutphen Elderly Study" 342 : 1007-1011, 1993

      34 Mattson MP, "Beta-Amyloid peptides destabilize calcium homeostasis and render human cortical neurons vulnerable to excitotoxicity" 12 : 376-389, 1992

      35 Moosmann B, "Antioxidants as treatment for neurodegenerative disorders" 11 : 1407-1435, 2002

      36 Robards K, "Analytical chemistry of fruit bioflavonoids. A review" 122 : 11R-34R, 1997

      37 Masters CL, "Amyloid plaque core protein in Alzheimer disease and Down syndrome" 82 : 4245-4249, 1985

      38 Small DH, "Alzheimer's disease and the amyloid beta protein: What is the role of amyloid?" 73 : 443-449, 1999

      39 Small DH, "Alzheimer's disease and Abeta toxicity: from top to bottom" 2 : 595-598, 2001

      40 Bisaglia M, "Acetaminophen protects hippocampal neurons and PC12cultures from amyloid beta-peptides induced oxidative stress and reduces NF-kappaB activation" 41 : 43-54, 2002

      41 Hensley K, "A model for beta-amyloid aggregation and neurotoxicity based on free radical generation by the peptide: relevance to Alzheimer disease" 91 : 3270-3274, 1994

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      학술지 이력

      학술지 이력
      연월일 이력구분 이력상세 등재구분
      2027 평가예정 재인증평가 신청대상 (재인증)
      2021-01-01 평가 등재학술지 유지 (재인증) KCI등재
      2018-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2015-01-01 평가 등재학술지 선정 (계속평가) KCI등재
      2013-01-01 평가 등재후보학술지 유지 (기타) KCI등재후보
      2012-01-01 평가 등재후보 1차 FAIL (등재후보1차) KCI등재후보
      2010-01-01 평가 등재후보학술지 선정 (신규평가) KCI등재후보
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      학술지 인용정보

      학술지 인용정보
      기준연도 WOS-KCI 통합IF(2년) KCIF(2년) KCIF(3년)
      2016 0.16 0.16 0.11
      KCIF(4년) KCIF(5년) 중심성지수(3년) 즉시성지수
      0.1 0.08 0.34 0.06
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