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dc.contributor.authorTomita, Michiyoen_US
dc.contributor.authorHolman, Brita Jen_US
dc.contributor.authorSantoro, Christopher Pen_US
dc.contributor.authorSantoro, Thomas Jen_US
dc.date.accessioned2012-01-09T20:58:38Z
dc.date.available2012-01-09T20:58:38Z
dc.date.copyright2005
dc.date.issued2005-2-25
dc.identifier.citationTomita, Michiyo, Brita J Holman, Christopher P Santoro, Thomas J Santoro. "Astrocyte production of the chemokine macrophage inflammatory protein-2 is inhibited by the spice principle curcumin at the level of gene transcription" Journal of Neuroinflammation 2:8. (2005)
dc.identifier.issn1742-2094
dc.identifier.urihttps://hdl.handle.net/2144/2938
dc.description.abstractBACKGROUND In neuropathological processes associated with neutrophilic infiltrates, such as experimental allergic encephalitis and traumatic injury of the brain, the CXC chemokine, macrophage inflammatory protein-2 (MIP-2) is thought to play a pivotal role in the induction and perpetuation of inflammation in the central nervous system (CNS). The origin of MIP-2 in inflammatory disorders of the brain has not been fully defined but astrocytes appear to be a dominant source of this chemokine. Curcumin is a spice principle in, and constitutes approximately 4 percent of, turmeric. Curcumin's immunomodulating and antioxidant activities suggest that it might be a useful adjunct in the treatment of neurodegenerative illnesses characterized by inflammation. Relatively unexplored, but relevant to its potential therapeutic efficacy in neuroinflammatory syndromes is the effect of curcumin on chemokine production. To examine the possibility that curcumin may influence CNS inflammation by mechanisms distinct from its known anti-oxidant activities, we studied the effect of this spice principle on the synthesis of MIP-2 by astrocytes. METHODS Primary astrocytes were prepared from neonatal brains of CBA/CaJ mice. The cells were stimulated with lipopolysaccharide in the presence or absence of various amount of curcumin or epigallocatechin gallate. MIP-2 mRNA was analyzed using semi-quantitative PCR and MIP-2 protein production in the culture supernatants was quantified by ELISA. Astrocytes were transfected with a MIP-2 promoter construct, pGL3-MIP-2, and stimulated with lipopolysaccharide in the presence or absence of curcumin. RESULTS The induction of MIP-2 gene expression and the production of MIP-2 protein were inhibited by curcumin. Curcumin also inhibited lipopolysaccharide-induced transcription of the MIP-2 promoter reporter gene construct in primary astrocytes. However MIP-2 gene induction by lipopolysaccharide was not inhibited by another anti-oxidant, epigallocatechin gallate. CONCLUSION Our results indicate that curcumin potently inhibits MIP-2 production at the level of gene transcription and offer further support for its potential use in the treatment of inflammatory conditions of the CNS.en_US
dc.description.sponsorshipNorth Central Chapter of the Arthritis Foundationen_US
dc.language.isoen
dc.publisherBioMed Centralen_US
dc.rightsCopyright 2005 Tomita et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.en_US
dc.rights.urihttp://creativecommons.org/licenses/by/2.0
dc.subjectMIP-2en_US
dc.subjectAstrocytesen_US
dc.subjectCurcuminen_US
dc.subjectGene transcriptionen_US
dc.subjectChemokinesen_US
dc.subjectInflammationen_US
dc.titleAstrocyte Production of the Chemokine Macrophage Inflammatory Protein-2 Is Inhibited by the Spice Principle Curcumin at the Level of Gene Transcriptionen_US
dc.typeArticleen_US
dc.identifier.doi10.1186/1742-2094-2-8
dc.identifier.pmid15733321
dc.identifier.pmcid553992


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Copyright 2005 Tomita et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Except where otherwise noted, this item's license is described as Copyright 2005 Tomita et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.