| pubmed-article:10666520 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10666520 | lifeskim:mentions | umls-concept:C0079189 | lld:lifeskim |
| pubmed-article:10666520 | lifeskim:mentions | umls-concept:C0458247 | lld:lifeskim |
| pubmed-article:10666520 | lifeskim:mentions | umls-concept:C1314939 | lld:lifeskim |
| pubmed-article:10666520 | pubmed:issue | 2-3 | lld:pubmed |
| pubmed-article:10666520 | pubmed:dateCreated | 2000-3-16 | lld:pubmed |
| pubmed-article:10666520 | pubmed:abstractText | Dynorphin A is an endogenous opioid peptide, which has previously been shown to produce a long-lasting allodynia and hyperalgesia in mice, behavioral states consistent with signs of clinically observed neuropathic pain. This dynorphin-induced allodynia was used as a pharmacological, central model of neuropathic pain. In this study, we examined the involvement of the cytokine IL-1beta, the transcription factor nuclear factor kappa B (NF-kappaB), and de novo protein synthesis in the development of allodynia induced by intrathecal (i.t.) administration of dynorphin in male ICR mice. Pretreatment with the protein synthesis inhibitor cycloheximide (0. 3-85nmol), the NF-kappaB inhibitor pyrrolidinedithiocarbamate (PDTC) (0.001-1000pmol), the IL-1 receptor antagonist (IL-1ra) protein (0. 01-100ng), the caspase-1 inhibitor (YVAD) (0.1-300pmol), and the anti-inflammatory cytokine IL-10 (0.1-300ng) all dose-dependently reduced the induction of dynorphin-induced allodynia. Finally, IL-10 administered within the first 24h after the dynorphin insult prevented the development of chronic allodynia. These results demonstrate that the anti-inflammatory cytokines IL-10 and IL-1ra impede the development of dynorphin-induced allodynia. These results also suggest that production of new proteins through NF-kappaB activation is required for the induction of allodynia. We speculate that IL-1ra, IL-10, PDTC and cycloheximide interfere with the central pro-inflammatory cascade. Modulation of cytokine activity in the spinal cord may therefore prove to be an effective therapeutic strategy for the treatment of chronic pain. | lld:pubmed |
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| pubmed-article:10666520 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10666520 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10666520 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:10666520 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10666520 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:10666520 | pubmed:issn | 0304-3959 | lld:pubmed |
| pubmed-article:10666520 | pubmed:author | pubmed-author:WilcoxG LGL | lld:pubmed |
| pubmed-article:10666520 | pubmed:author | pubmed-author:YezierskiR... | lld:pubmed |
| pubmed-article:10666520 | pubmed:author | pubmed-author:BetheaJ RJR | lld:pubmed |
| pubmed-article:10666520 | pubmed:author | pubmed-author:LaughlinT MTM | lld:pubmed |
| pubmed-article:10666520 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10666520 | pubmed:volume | 84 | lld:pubmed |
| pubmed-article:10666520 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10666520 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10666520 | pubmed:pagination | 159-67 | lld:pubmed |
| pubmed-article:10666520 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:10666520 | pubmed:meshHeading | pubmed-meshheading:10666520... | lld:pubmed |
| pubmed-article:10666520 | pubmed:year | 2000 | lld:pubmed |
| pubmed-article:10666520 | pubmed:articleTitle | Cytokine involvement in dynorphin-induced allodynia. | lld:pubmed |
| pubmed-article:10666520 | pubmed:affiliation | Department of Pharmacology, University of Minnesota, Minneapolis 55455, USA. | lld:pubmed |
| pubmed-article:10666520 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10666520 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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