Neuroprotective Effects of Naturally Occurring Polyphenols on Quinolinic Acid-induced Excitotoxicity in Human Neurons

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avondale-bepress-to-dspace.facultyNursing
avondale-bepress-to-dspace.peer_review_statusPeer reviewed before publication
avondale-bepress.abstract<p>Quinolinic acid (QUIN) excitotoxicity is mediated by elevated intracellular Ca<sup>2+</sup> levels, and nitric oxide-mediated oxidative stress, resulting in DNA damage, poly(ADP-ribose) polymerase (PARP) activation, NAD<sup>+</sup> depletion and cell death. We evaluated the effect of a series of polyphenolic compounds [i.e. epigallocatechin gallate (EPCG), catechin hydrate, curcumin, apigenin, naringenin and gallotannin] with antioxidant properties on QUIN-induced excitotoxicity on primary cultures of human neurons. We showed that the polyphenols, EPCG, catechin hydrate and curcumin can attenuate QUIN-induced excitotoxicity to a greater extent than apigenin, naringenin and gallotannin. Both EPCG and curcumin were able to attenuate QUIN-induced Ca<sup>2+</sup> influx and neuronal nitric oxide synthase (nNOS) activity to a greater extent compared with apigenin, naringenin and gallotannin. Although Ca<sup>2+</sup> influx was not attenuated by catechin hydrate, nNOS activity was reduced, probably through direct inhibition of the enzyme. All polyphenols reduced the oxidative effects of increased nitric oxide production, thereby reducing the formation of 3-nitrotyrosine and poly (ADP-ribose) polymerase activity and, hence, preventing NAD<sup>+</sup> depletion and cell death. In addition to the well-known antioxidant properties of these natural phytochemicals, the inhibitory effect of some of these compounds on specific excitotoxic processes, such as Ca<sup>2+</sup> influx, provides additional evidence for the beneficial health effects of polyphenols in excitable tissue, particularly within the central nervous system.</p>
avondale-bepress.articleid1018
avondale-bepress.authorsNady Braidy
avondale-bepress.authorsRoss Grant
avondale-bepress.authorsSeray Adams
avondale-bepress.authorsGilles Guillemin
avondale-bepress.context-key3414168
avondale-bepress.coverpage-urlhttps://research.avondale.edu.au/nh_papers/19
avondale-bepress.document-typearticle
avondale-bepress.field.author_faculty_disciplineNursing
avondale-bepress.field.comments<p>Used by permission: The Authors.</p>
avondale-bepress.field.create_openurltrue
avondale-bepress.field.custom_citation<p>Braidy, N., Grant, R., Adams, S., & Guillemin, G. (2010). Neuroprotective effects of naturally occurring polyphenols on quinolinic acid-induced excitotoxicity in human neurons. <em>The FEBS Journal</em>, <em>277</em>(2), 368–382. doi:10.1111/j.1742-4658.2009.07487.x</p>
avondale-bepress.field.doihttps://doi.org/10.1111/j.1742-4658.2009.07487.x
avondale-bepress.field.embargo_date2012-10-21T00:00:00Z
avondale-bepress.field.issn1742-4658
avondale-bepress.field.issue_number2
avondale-bepress.field.journalThe FEBS Journal
avondale-bepress.field.page_numbers368-382
avondale-bepress.field.peer_reviewBefore publication
avondale-bepress.field.publication_date2010-01-01T00:00:00Z
avondale-bepress.field.source_fulltext_urlhttp://onlinelibrary.wiley.com/doi/10.1111/j.1742-4658.2009.07487.x/pdf
avondale-bepress.field.source_publication<p>This article was originally published as:</p> <p>Braidy, N., Grant, R., Adams, S., & Guillemin, G. (2010). Neuroprotective effects of naturally occurring polyphenols on quinolinic acid-induced excitotoxicity in human neurons. <em>The FEBS Journal</em>, <em>277</em>(2), 368–382.doi:10.1111/j.1742-4658.2009.07487.x</p><p>ISSN:1742-4658</p>
avondale-bepress.field.volume_number277
avondale-bepress.fulltext-urlhttps://research.avondale.edu.au/cgi/viewcontent.cgi?article=1018&amp;context=nh_papers&amp;unstamped=1
avondale-bepress.keywordsAlzheimer’s disease
avondale-bepress.keywordsexcitotoxicity
avondale-bepress.keywordsNAD+
avondale-bepress.keywordspolyphenols
avondale-bepress.keywordsquinolinic acid
avondale-bepress.label19
avondale-bepress.publication-date2010-01-01T00:00:00Z
avondale-bepress.publication-titleNursing and Health Papers and Journal Articles
avondale-bepress.statepublished
avondale-bepress.submission-date2012-10-21T22:38:13Z
avondale-bepress.submission-pathnh_papers/19
avondale-bepress.titleNeuroprotective Effects of Naturally Occurring Polyphenols on Quinolinic Acid-induced Excitotoxicity in Human Neurons
avondale-bepress.typearticle
dc.contributor.authorGuillemin, Gilles
dc.contributor.authorAdams, Seray
dc.contributor.authorGrant, Ross
dc.contributor.authorBraidy, Nady
dc.date.accessioned2023-11-01T00:27:23Z
dc.date.available2023-11-01T00:27:23Z
dc.date.issued2010-01-01
dc.date.submitted2012-10-21T22:38:13Z
dc.description.abstract<p>Quinolinic acid (QUIN) excitotoxicity is mediated by elevated intracellular Ca<sup>2+</sup> levels, and nitric oxide-mediated oxidative stress, resulting in DNA damage, poly(ADP-ribose) polymerase (PARP) activation, NAD<sup>+</sup> depletion and cell death. We evaluated the effect of a series of polyphenolic compounds [i.e. epigallocatechin gallate (EPCG), catechin hydrate, curcumin, apigenin, naringenin and gallotannin] with antioxidant properties on QUIN-induced excitotoxicity on primary cultures of human neurons. We showed that the polyphenols, EPCG, catechin hydrate and curcumin can attenuate QUIN-induced excitotoxicity to a greater extent than apigenin, naringenin and gallotannin. Both EPCG and curcumin were able to attenuate QUIN-induced Ca<sup>2+</sup> influx and neuronal nitric oxide synthase (nNOS) activity to a greater extent compared with apigenin, naringenin and gallotannin. Although Ca<sup>2+</sup> influx was not attenuated by catechin hydrate, nNOS activity was reduced, probably through direct inhibition of the enzyme. All polyphenols reduced the oxidative effects of increased nitric oxide production, thereby reducing the formation of 3-nitrotyrosine and poly (ADP-ribose) polymerase activity and, hence, preventing NAD<sup>+</sup> depletion and cell death. In addition to the well-known antioxidant properties of these natural phytochemicals, the inhibitory effect of some of these compounds on specific excitotoxic processes, such as Ca<sup>2+</sup> influx, provides additional evidence for the beneficial health effects of polyphenols in excitable tissue, particularly within the central nervous system.</p>
dc.description.versionBefore publication
dc.identifier.citation<p>Braidy, N., Grant, R., Adams, S., & Guillemin, G. (2010). Neuroprotective effects of naturally occurring polyphenols on quinolinic acid-induced excitotoxicity in human neurons. <em>The FEBS Journal</em>, <em>277</em>(2), 368–382. doi:10.1111/j.1742-4658.2009.07487.x</p>
dc.identifier.doihttps://doi.org/10.1111/j.1742-4658.2009.07487.x
dc.identifier.issn1742-4658
dc.identifier.urihttps://research.avondale.edu.au/handle/123456789/03414168
dc.language.isoen_us
dc.provenance<p>This article was originally published as:</p> <p>Braidy, N., Grant, R., Adams, S., & Guillemin, G. (2010). Neuroprotective effects of naturally occurring polyphenols on quinolinic acid-induced excitotoxicity in human neurons. <em>The FEBS Journal</em>, <em>277</em>(2), 368–382.doi:10.1111/j.1742-4658.2009.07487.x</p><p>ISSN:1742-4658</p>
dc.rights<p>Used by permission: The Authors.</p>
dc.subjectAlzheimer’s disease
dc.subjectexcitotoxicity
dc.subjectNAD+
dc.subjectpolyphenols
dc.subjectquinolinic acid
dc.titleNeuroprotective Effects of Naturally Occurring Polyphenols on Quinolinic Acid-induced Excitotoxicity in Human Neurons
dc.typeJournal Article
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