Quercetin, not caffeine, is a major neuroprotective component in coffee.
Identifieur interne : 000160 ( PubMed/Checkpoint ); précédent : 000159; suivant : 000161Quercetin, not caffeine, is a major neuroprotective component in coffee.
Auteurs : Moonhee Lee ; Edith G. Mcgeer ; Patrick L. Mcgeer [Canada]Source :
- Neurobiology of aging [ 1558-1497 ] ; 2016.
Abstract
Epidemiologic studies indicate that coffee consumption reduces the risk of Parkinson's disease and Alzheimer's disease. To determine the factors involved, we examined the protective effects of coffee components. The test involved prevention of neurotoxicity to SH-SY5Y cells that was induced by lipopolysaccharide plus interferon-γ or interferon-γ released from activated microglia and astrocytes. We found that quercetin, flavones, chlorogenic acid, and caffeine protected SH-SY5Y cells from these toxins. They also reduced the release of tumor necrosis factor-α and interleukin-6 from the activated microglia and astrocytes and attenuated the activation of proteins from P38 mitogen-activated protein kinase (MAPK) and nuclear factor kappa light chain enhancer of activated B cells (NFκB). After exposure to toxin containing glial-stimulated conditioned medium, we also found that quercetin reduced oxidative/nitrative damage to DNA, as well as to the lipids and proteins of SH-SY5Y cells. There was a resultant increase in [GSH]i in SH-SY5Y cells. The data indicate that quercetin is the major neuroprotective component in coffee against Parkinson's disease and Alzheimer's disease.
DOI: 10.1016/j.neurobiolaging.2016.06.015
PubMed: 27479153
Affiliations:
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Mcgeer</name><affiliation><nlm:affiliation>Kinsmen Laboratory of Neurological Research, University of British Columbia, Vancouver, British Columbia Canada.</nlm:affiliation><wicri:noCountry code="subField">British Columbia Canada</wicri:noCountry></affiliation></author><author><name sortKey="Mcgeer, Patrick L" sort="Mcgeer, Patrick L" uniqKey="Mcgeer P" first="Patrick L" last="Mcgeer">Patrick L. Mcgeer</name><affiliation wicri:level="1"><nlm:affiliation>Kinsmen Laboratory of Neurological Research, University of British Columbia, Vancouver, British Columbia Canada. Electronic address: mcgeerpl@mail.ubc.ca.</nlm:affiliation><country wicri:rule="url">Canada</country></affiliation></author></analytic><series><title level="j">Neurobiology of aging</title><idno type="eISSN">1558-1497</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Epidemiologic studies indicate that coffee consumption reduces the risk of Parkinson's disease and Alzheimer's disease. To determine the factors involved, we examined the protective effects of coffee components. The test involved prevention of neurotoxicity to SH-SY5Y cells that was induced by lipopolysaccharide plus interferon-γ or interferon-γ released from activated microglia and astrocytes. We found that quercetin, flavones, chlorogenic acid, and caffeine protected SH-SY5Y cells from these toxins. They also reduced the release of tumor necrosis factor-α and interleukin-6 from the activated microglia and astrocytes and attenuated the activation of proteins from P38 mitogen-activated protein kinase (MAPK) and nuclear factor kappa light chain enhancer of activated B cells (NFκB). After exposure to toxin containing glial-stimulated conditioned medium, we also found that quercetin reduced oxidative/nitrative damage to DNA, as well as to the lipids and proteins of SH-SY5Y cells. There was a resultant increase in [GSH]i in SH-SY5Y cells. The data indicate that quercetin is the major neuroprotective component in coffee against Parkinson's disease and Alzheimer's disease.</div></front></TEI><pubmed><MedlineCitation Status="In-Process" Owner="NLM"><PMID Version="1">27479153</PMID><DateCreated><Year>2016</Year><Month>09</Month><Day>11</Day></DateCreated><DateRevised><Year>2016</Year><Month>09</Month><Day>11</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1558-1497</ISSN><JournalIssue CitedMedium="Internet"><Volume>46</Volume><PubDate><Year>2016</Year><Month>Oct</Month></PubDate></JournalIssue><Title>Neurobiology of aging</Title><ISOAbbreviation>Neurobiol. Aging</ISOAbbreviation></Journal><ArticleTitle>Quercetin, not caffeine, is a major neuroprotective component in coffee.</ArticleTitle><Pagination><MedlinePgn>113-23</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.neurobiolaging.2016.06.015</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0197-4580(16)30115-4</ELocationID><Abstract><AbstractText>Epidemiologic studies indicate that coffee consumption reduces the risk of Parkinson's disease and Alzheimer's disease. To determine the factors involved, we examined the protective effects of coffee components. The test involved prevention of neurotoxicity to SH-SY5Y cells that was induced by lipopolysaccharide plus interferon-γ or interferon-γ released from activated microglia and astrocytes. We found that quercetin, flavones, chlorogenic acid, and caffeine protected SH-SY5Y cells from these toxins. They also reduced the release of tumor necrosis factor-α and interleukin-6 from the activated microglia and astrocytes and attenuated the activation of proteins from P38 mitogen-activated protein kinase (MAPK) and nuclear factor kappa light chain enhancer of activated B cells (NFκB). After exposure to toxin containing glial-stimulated conditioned medium, we also found that quercetin reduced oxidative/nitrative damage to DNA, as well as to the lipids and proteins of SH-SY5Y cells. There was a resultant increase in [GSH]i in SH-SY5Y cells. The data indicate that quercetin is the major neuroprotective component in coffee against Parkinson's disease and Alzheimer's disease.</AbstractText><CopyrightInformation>Copyright © 2016 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Moonhee</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Kinsmen Laboratory of Neurological Research, University of British Columbia, Vancouver, British Columbia Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>McGeer</LastName><ForeName>Edith G</ForeName><Initials>EG</Initials><AffiliationInfo><Affiliation>Kinsmen Laboratory of Neurological Research, University of British Columbia, Vancouver, British Columbia Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>McGeer</LastName><ForeName>Patrick L</ForeName><Initials>PL</Initials><AffiliationInfo><Affiliation>Kinsmen Laboratory of Neurological Research, University of British Columbia, Vancouver, British Columbia Canada. 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