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Inhibitory effects of long-term administration of ferulic acid on astrocyte activation induced by intracerebroventricular injection of beta-amyloid peptide (1-42) in mice.

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dc.contributor.authorCho, JY-
dc.contributor.authorKim, HS-
dc.contributor.authorKim, DH-
dc.contributor.authorYan, JJ-
dc.contributor.authorSuh, HW-
dc.contributor.authorSong, DK-
dc.date.accessioned2011-07-11T04:37:40Z-
dc.date.available2011-07-11T04:37:40Z-
dc.date.issued2005-
dc.identifier.issn0278-5846-
dc.identifier.urihttp://repository.ajou.ac.kr/handle/201003/3265-
dc.description.abstractAccumulating evidence indicates that glial cells are actively involved in the pathogenesis of Alzheimer's disease. We recently reported protective effects of long-term administration of ferulic acid against learning and memory deficit induced by centrally administered beta-amyloid peptide (Abeta)1-42 in mice. In that report, we found that the Abeta1-42-induced increases in immunoreactivities of glial fibrillary acidic protein, the astrocyte marker, and interleukin(IL)-1beta in the hippocampus are also suppressed by pretreatment with ferulic acid. In the present study, we aimed to further characterize the effect of long-term administration of ferulic acid on the centrally administered Abeta1-42-induced activation of glial cells in mice. Mice were allowed free access to drinking water (control) or water containing ferulic acid (0.006%) for 4 weeks, and then Abeta1-42 (410 pmol) was administered via intracerebroventricular injection. Intracerebroventricularly injected Abeta1-42 induced an increase in immunoreactivities of endothelial nitric oxide synthase (eNOS) and 3-nitrotyrosine (3-NT) in the activated astrocytes in the hippocampus. Pretreatment of ferulic acid for 4 weeks prevented the Abeta1-42-induced increase in eNOS and 3-NT immunoreactivities. Administration of ferulic acid per se induced a transient and slight increase in eNOS immunoreactivity in the hippocampus on day 14, which returned to basal levels on day 28. Intracerebroventricularly injected Abeta1-42 also increased interleukin-1alpha(IL-1alpha) immunoreactivity in the hippocampus, which was also suppressed by pretreatment with ferulic acid. These results demonstrate that long-term administration of ferulic acid induces suppression of the centrallly injected Abeta1-42-induced activation of astrocytes which is suggested to underlie the protective effect of ferulic acid against Abeta1-42 toxicity in vivo.-
dc.language.isoen-
dc.subject.MESHAmyloid beta-Peptides-
dc.subject.MESHAnimals-
dc.subject.MESHAstrocytes-
dc.subject.MESHCell Count-
dc.subject.MESHCoumaric Acids-
dc.subject.MESHDrug Interactions-
dc.subject.MESHFree Radical Scavengers-
dc.subject.MESHGene Expression Regulation-
dc.subject.MESHGlial Fibrillary Acidic Protein-
dc.subject.MESHHippocampus-
dc.subject.MESHImmunohistochemistry-
dc.subject.MESHInjections, Intraventricular-
dc.subject.MESHInterleukin-1-
dc.subject.MESHMale-
dc.subject.MESHMice-
dc.subject.MESHMice, Inbred ICR-
dc.subject.MESHNitric Oxide Synthase-
dc.subject.MESHNitric Oxide Synthase Type II-
dc.subject.MESHNitric Oxide Synthase Type III-
dc.subject.MESHPeptide Fragments-
dc.subject.MESHTime Factors-
dc.subject.MESHTyrosine-
dc.titleInhibitory effects of long-term administration of ferulic acid on astrocyte activation induced by intracerebroventricular injection of beta-amyloid peptide (1-42) in mice.-
dc.typeArticle-
dc.identifier.pmid15970368-
dc.identifier.urlhttp://linkinghub.elsevier.com/retrieve/pii/S0278-5846(05)00141-7-
dc.contributor.affiliatedAuthor조, 제영-
dc.type.localJournal Papers-
dc.identifier.doi10.1016/j.pnpbp.2005.04.022-
dc.citation.titleProgress in neuro-psychopharmacology & biological psychiatry-
dc.citation.volume29-
dc.citation.number6-
dc.citation.date2005-
dc.citation.startPage901-
dc.citation.endPage907-
dc.identifier.bibliographicCitationProgress in neuro-psychopharmacology & biological psychiatry, 29(6). : 901-907, 2005-
dc.identifier.eissn1878-4216-
dc.relation.journalidJ002785846-
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Journal Papers > Research Organization > Research Institute for Neural Science & Technology
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