Protective effects of caffeic acid phenethyl ester against experimental allergic encephalomyelitis-induced oxidative stress in rats

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dc.authoridArmutcu, Ferah/0000-0002-3218-9480;
dc.authorwosidArmutcu, Ferah/A-1364-2019
dc.authorwosidOztas, Emin/B-5730-2016
dc.contributor.authorIlhan, A
dc.contributor.authorAkyol, O
dc.contributor.authorGurel, A
dc.contributor.authorArmutcu, F
dc.contributor.authorIraz, M
dc.contributor.authorOztas, E
dc.date.accessioned2024-08-04T20:15:11Z
dc.date.available2024-08-04T20:15:11Z
dc.date.issued2004
dc.departmentİnönü Üniversitesien_US
dc.description.abstractBecause oxidative damage has been known to be involved in inflammatory and autoimmune-mediated tissue destruction, modulation of oxygen free radical production represents a new approach to the treatment of inflammatory and autoimmune diseases. Central nervous system tissue is particularly vulnerable to oxidative damage, suggesting that oxidation plays an important role in the pathogenesis of multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE). Caffeic acid phenethyl ester (CAPE), an active component of honeybee propolis, has been determined to have antioxidant, anti-inflammatory, antiviral, and anticancer activities. We have previously reported that CAPE inhibits ischemia-reperfusion injury and oxidative stress in rabbit spinal cord tissue. The present study, therefore, examined effects of CAPE on oxidative tissue damage in EAE in rats. Treatment with CAPE significantly inhibited reactive oxygen species (ROS) production induced by EAE, and ameliorated clinical symptoms in rats. These results suggest that CAPE may exert its anti-inflammatory effect by inhibiting ROS production at the transcriptional level through the suppression of nuclear factor kappaB activation, and by directly inhibiting the catalytic activity of inducible nitric oxide synthase. (C) 2004 Elsevier Inc. All rights reserved.en_US
dc.identifier.doi10.1016/j.freeradbiomed.2004.04.022
dc.identifier.endpage394en_US
dc.identifier.issn0891-5849
dc.identifier.issn1873-4596
dc.identifier.issue3en_US
dc.identifier.pmid15223072en_US
dc.identifier.scopus2-s2.0-3042528284en_US
dc.identifier.scopusqualityQ1en_US
dc.identifier.startpage386en_US
dc.identifier.urihttps://doi.org/10.1016/j.freeradbiomed.2004.04.022
dc.identifier.urihttps://hdl.handle.net/11616/94212
dc.identifier.volume37en_US
dc.identifier.wosWOS:000222740800010en_US
dc.identifier.wosqualityQ1en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherElsevier Science Incen_US
dc.relation.ispartofFree Radical Biology and Medicineen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectcaffeic acid phenethyl esteren_US
dc.subjectexperimental autoimmune encephalomyelitisen_US
dc.subjectspinal corden_US
dc.subjectoxidative stressen_US
dc.subjectneurologic outcomeen_US
dc.subjectfree radicalsen_US
dc.titleProtective effects of caffeic acid phenethyl ester against experimental allergic encephalomyelitis-induced oxidative stress in ratsen_US
dc.typeArticleen_US

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