Publication:
Curcumin i mediates neuroprotective effect through attenuation of quinoprotein formation, p-p38 MAPK expression, and caspase-3 activation in 6-hydroxydopamine treated SH-SY5Y cells

dc.contributor.authorBenjawan Meesarapeeen_US
dc.contributor.authorAnusorn Thampithaken_US
dc.contributor.authorYamaratee Jaisinen_US
dc.contributor.authorPimtip Sanvarindaen_US
dc.contributor.authorApichart Suksamrarnen_US
dc.contributor.authorPatoomratana Tuchindaen_US
dc.contributor.authorNoppawan Phumala Moralesen_US
dc.contributor.authorYupin Sanvarindaen_US
dc.contributor.otherMahidol Universityen_US
dc.contributor.otherBurapha Universityen_US
dc.contributor.otherSrinakharinwirot Universityen_US
dc.contributor.otherRamkhamhaeng Universityen_US
dc.date.accessioned2018-11-09T03:11:32Z
dc.date.available2018-11-09T03:11:32Z
dc.date.issued2014-01-01en_US
dc.description.abstract6-Hydroxydopamine (6-OHDA) selectively enters dopaminergic neurons and undergoes auto-oxidation resulting in the generation of reactive oxygen species and dopamine quinones, subsequently leading to apoptosis. This mechanism mimics the pathogenesis of Parkinson's disease and has been used to induce experimental Parkinsonism in both in vitro and in vivo systems. In this study, we investigated the effects of curcumin I (diferuloylmethane) purified from Curcuma longa on quinoprotein production, phosphorylation of p38 MAPK (p-p38), and caspase-3 activation in 6-OHDA-treated SH-SY5Y dopaminergic cells. Pretreatment of SH-SY5Y with curcumin I at concentrations of 1, 5, 10, and 20 μM, significantly decreased the formation of quinoprotein and reduced the levels of p-p38 and cleaved caspase-3 in a dose-dependent manner. Moreover, the levels of the dopaminergic neuron marker, phospho-tyrosine hydroxylase (p-TH), were also dose-dependently increased upon treatment with curcumin I. Our results clearly demonstrated that curcumin I protects neurons against oxidative damage, as shown by attenuation of p-p38 expression, caspase-3-activation, and toxic quinoprotein formation, together with the restoration of p-TH levels. This study provides evidence for the therapeutic potential of curcumin I in the chemoprevention of oxidative stress-related neurodegeneration. Copyright © 2013 John Wiley & Sons, Ltd.en_US
dc.identifier.citationPhytotherapy Research. Vol.28, No.4 (2014), 611-616en_US
dc.identifier.doi10.1002/ptr.5036en_US
dc.identifier.issn10991573en_US
dc.identifier.issn0951418Xen_US
dc.identifier.other2-s2.0-84898011829en_US
dc.identifier.urihttps://repository.li.mahidol.ac.th/handle/20.500.14594/34919
dc.rightsMahidol Universityen_US
dc.rights.holderSCOPUSen_US
dc.source.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84898011829&origin=inwarden_US
dc.subjectPharmacology, Toxicology and Pharmaceuticsen_US
dc.titleCurcumin i mediates neuroprotective effect through attenuation of quinoprotein formation, p-p38 MAPK expression, and caspase-3 activation in 6-hydroxydopamine treated SH-SY5Y cellsen_US
dc.typeArticleen_US
dspace.entity.typePublication
mu.datasource.scopushttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84898011829&origin=inwarden_US

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