| pubmed-article:20051658 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20051658 | lifeskim:mentions | umls-concept:C0003864 | lld:lifeskim |
| pubmed-article:20051658 | lifeskim:mentions | umls-concept:C1280500 | lld:lifeskim |
| pubmed-article:20051658 | lifeskim:mentions | umls-concept:C0231491 | lld:lifeskim |
| pubmed-article:20051658 | lifeskim:mentions | umls-concept:C0968253 | lld:lifeskim |
| pubmed-article:20051658 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:20051658 | pubmed:dateCreated | 2010-1-22 | lld:pubmed |
| pubmed-article:20051658 | pubmed:abstractText | It was investigated whether the C3a-receptor antagonist (C3aRA) SB 290157 was involved in the suppression of anti-OVA pAb-induced arthritis because it is well known that anaphylatoxin C3a plays a crucial role in the development of an effective inflammatory response during complement activation. Anti-OVA pAb-induced arthritis was induced in DBA/1J mice by administration of anti-OVA pAb 0.5 h prior to intra-articular (i.a.) injection of OVA (0 h). Two peaks of joint swelling were observed at 0.5 and 3 h. The role of C3aRA in arthritis was investigated by injection of SB 290157 at concentrations of 10 and 30 mg/kg at 0 and 2 h. The antagonist was able to reduce joint swelling only at 3 h, and about 50% inhibition of joint swelling was observed with the concentration of 30 mg/kg. The C3 level was significantly decreased at 3 h compared with naïve mice showing complement consumption. Furthermore, the C3 activation was observed and increased corresponding to the graded concentration of anti-OVA pAb. The results also revealed that the C3aRA was able to reduce the expression of IL-1beta in synovial tissue. Taken together, the results suggested that C3aRA may be effective in the inhibition of arthritis. | lld:pubmed |
| pubmed-article:20051658 | pubmed:language | eng | lld:pubmed |
| pubmed-article:20051658 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20051658 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:20051658 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20051658 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20051658 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20051658 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20051658 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20051658 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20051658 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:20051658 | pubmed:issn | 1347-8648 | lld:pubmed |
| pubmed-article:20051658 | pubmed:author | pubmed-author:YoshinoShinS | lld:pubmed |
| pubmed-article:20051658 | pubmed:author | pubmed-author:MizutaniNobua... | lld:pubmed |
| pubmed-article:20051658 | pubmed:author | pubmed-author:OgawaNaokiN | lld:pubmed |
| pubmed-article:20051658 | pubmed:author | pubmed-author:HutamekalinPi... | lld:pubmed |
| pubmed-article:20051658 | pubmed:author | pubmed-author:TakedaKoheiK | lld:pubmed |
| pubmed-article:20051658 | pubmed:author | pubmed-author:TaniMitsuhiro... | lld:pubmed |
| pubmed-article:20051658 | pubmed:author | pubmed-author:TsugaYukoY | lld:pubmed |
| pubmed-article:20051658 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:20051658 | pubmed:volume | 112 | lld:pubmed |
| pubmed-article:20051658 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:20051658 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:20051658 | pubmed:pagination | 56-63 | lld:pubmed |
| pubmed-article:20051658 | pubmed:dateRevised | 2011-6-20 | lld:pubmed |
| pubmed-article:20051658 | pubmed:meshHeading | pubmed-meshheading:20051658... | lld:pubmed |
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| pubmed-article:20051658 | pubmed:meshHeading | pubmed-meshheading:20051658... | lld:pubmed |
| pubmed-article:20051658 | pubmed:year | 2010 | lld:pubmed |
| pubmed-article:20051658 | pubmed:articleTitle | Effect of the C3a-receptor antagonist SB 290157 on anti-OVA polyclonal antibody-induced arthritis. | lld:pubmed |
| pubmed-article:20051658 | pubmed:affiliation | Department of Pharmacology, Kobe Pharmaceutical University, Japan. | lld:pubmed |
| pubmed-article:20051658 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:20051658 | pubmed:publicationType | Comparative Study | lld:pubmed |
| pubmed-article:20051658 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
