pubmed-article:18761708 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:18761708 | lifeskim:mentions | umls-concept:C1565860 | lld:lifeskim |
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pubmed-article:18761708 | lifeskim:mentions | umls-concept:C0012472 | lld:lifeskim |
pubmed-article:18761708 | lifeskim:mentions | umls-concept:C0079904 | lld:lifeskim |
pubmed-article:18761708 | lifeskim:mentions | umls-concept:C0441655 | lld:lifeskim |
pubmed-article:18761708 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
pubmed-article:18761708 | lifeskim:mentions | umls-concept:C1367731 | lld:lifeskim |
pubmed-article:18761708 | lifeskim:mentions | umls-concept:C1150587 | lld:lifeskim |
pubmed-article:18761708 | lifeskim:mentions | umls-concept:C1705632 | lld:lifeskim |
pubmed-article:18761708 | lifeskim:mentions | umls-concept:C0030685 | lld:lifeskim |
pubmed-article:18761708 | lifeskim:mentions | umls-concept:C0680255 | lld:lifeskim |
pubmed-article:18761708 | lifeskim:mentions | umls-concept:C0391871 | lld:lifeskim |
pubmed-article:18761708 | lifeskim:mentions | umls-concept:C1283071 | lld:lifeskim |
pubmed-article:18761708 | lifeskim:mentions | umls-concept:C1963578 | lld:lifeskim |
pubmed-article:18761708 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
pubmed-article:18761708 | lifeskim:mentions | umls-concept:C0077274 | lld:lifeskim |
pubmed-article:18761708 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
pubmed-article:18761708 | pubmed:issue | 3 | lld:pubmed |
pubmed-article:18761708 | pubmed:dateCreated | 2008-11-7 | lld:pubmed |
pubmed-article:18761708 | pubmed:abstractText | Activated microglia participate in neuroinflammation which contributes to neuronal damage in neurodegenerative diseases. Inhibition of microglial activation may have potential anti-inflammatory effects. Our laboratory has previously reported that triptolide, a natural biologically active compound extracted from Tripterygium wilfordii, could protect dopaminergic neurons from inflammation-mediated damage. However, the mechanism by which triptolide inhibits inflammation remains unknown. We reported here that inhibition of prostaglandin E(2) (PGE(2)) production could be a potential mechanism of triptolide to suppress inflammation. Triptolide suppressed c-jun NH2-terminal kinase (JNK) phosphorylation, cyclooxygenase 2 (COX-2) expression and PGE(2) production in microglial cultures treated with lipopolysaccharide (LPS). Triptolide also greatly inhibited the transcriptional activity, but not the DNA-binding activity of nuclear factor-kappaB (NF-kappaB) in microglia following LPS stimulation. These results indicate that triptolide might suppress NF-kappaB activity to down-regulate COX-2 expression. The LPS-stimulated transcriptional activity of NF-kappaB was suppressed by inhibition of p38MAPK, but not by that of JNK and extracellular signal-regulated kinase. Furthermore, the LPS-induced PGE(2) production was reduced by inhibiting these kinases. Taken together, these results suggest that triptolide may suppress neuroinflammation via a mechanism that involves inactivation of two parallel signaling pathways: p38-NF-kappaB-COX-2-PGE(2) and JNK-PGE(2). | lld:pubmed |
pubmed-article:18761708 | pubmed:language | eng | lld:pubmed |
pubmed-article:18761708 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18761708 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:18761708 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18761708 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18761708 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:18761708 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18761708 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18761708 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:18761708 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:18761708 | pubmed:month | Nov | lld:pubmed |
pubmed-article:18761708 | pubmed:issn | 1471-4159 | lld:pubmed |
pubmed-article:18761708 | pubmed:author | pubmed-author:BCC | lld:pubmed |
pubmed-article:18761708 | pubmed:author | pubmed-author:XueBingB | lld:pubmed |
pubmed-article:18761708 | pubmed:author | pubmed-author:WangXiaominX | lld:pubmed |
pubmed-article:18761708 | pubmed:author | pubmed-author:GongYuntaoY | lld:pubmed |
pubmed-article:18761708 | pubmed:author | pubmed-author:JingLimingL | lld:pubmed |
pubmed-article:18761708 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:18761708 | pubmed:volume | 107 | lld:pubmed |
pubmed-article:18761708 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:18761708 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:18761708 | pubmed:pagination | 779-88 | lld:pubmed |
pubmed-article:18761708 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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pubmed-article:18761708 | pubmed:year | 2008 | lld:pubmed |
pubmed-article:18761708 | pubmed:articleTitle | Triptolide inhibits COX-2 expression and PGE2 release by suppressing the activity of NF-kappaB and JNK in LPS-treated microglia. | lld:pubmed |
pubmed-article:18761708 | pubmed:affiliation | Department of Neurobiology, School of Basic Medical Sciences, Peking University Health Science Center, Ministry of Education, Key Laboratory for Neuroscience, Beijing, China. | lld:pubmed |
pubmed-article:18761708 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:18761708 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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