| pubmed-article:20061538 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20061538 | lifeskim:mentions | umls-concept:C0018787 | lld:lifeskim |
| pubmed-article:20061538 | lifeskim:mentions | umls-concept:C0031621 | lld:lifeskim |
| pubmed-article:20061538 | lifeskim:mentions | umls-concept:C0243026 | lld:lifeskim |
| pubmed-article:20061538 | lifeskim:mentions | umls-concept:C0277785 | lld:lifeskim |
| pubmed-article:20061538 | lifeskim:mentions | umls-concept:C1336634 | lld:lifeskim |
| pubmed-article:20061538 | lifeskim:mentions | umls-concept:C0023688 | lld:lifeskim |
| pubmed-article:20061538 | lifeskim:mentions | umls-concept:C0599946 | lld:lifeskim |
| pubmed-article:20061538 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:20061538 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:20061538 | pubmed:dateCreated | 2010-2-25 | lld:pubmed |
| pubmed-article:20061538 | pubmed:abstractText | Myocardial dysfunction is a major consequence of septic shock and contributes to the high mortality of sepsis. In the present study, we examined the effect of Toll-like receptor 2 (TLR2) ligands, peptidoglycan (PGN), and Pam3CSK4 (Pam3) on cardiac function in cecal ligation and puncture (CLP)-induced sepsis in mice. We also investigated whether the phosphoinositide 3-kinase (PI3K)/Akt signaling pathway is involved in the effect of TLR2 ligands on cardiac function in CLP mice. PGN was administered to C57B6/L mice 1 h before the induction of CLP. Sham surgically operated mice served as a control. Cardiac function indexes (rate of change in left ventricular pressure, stroke work, cardiac output, and ejection fraction) were examined by a microconductance pressure catheter. Cardiac function was significantly decreased 6 h after CLP-induced sepsis compared with sham-operated control. In contrast, PGN administration attenuated CLP-induced cardiac dysfunction. Importantly, the therapeutic treatment with Pam3 1 h after CLP also significantly attenuated cardiac dysfunction in CLP mice. However, the beneficial effect of TLR2 ligands on cardiac dysfunction in CLP-mice was abolished in TLR2-deficient mice. PGN administration significantly increased the levels of phospho-Akt and phospho-GSK-3beta in the myocardium compared with the levels in untreated CLP mice. PI3K inhibition abolished the PGN-induced attenuation of cardiac dysfunction in CLP mice. In conclusion, these data demonstrate that the administration of TLR2 ligands, PGN, or Pam3 attenuates cardiac dysfunction in septic mice via a TLR2/PI3K-dependent mechanism. More significantly, Pam3 therapeutic treatment will have a potential clinical relevance. | lld:pubmed |
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| pubmed-article:20061538 | pubmed:language | eng | lld:pubmed |
| pubmed-article:20061538 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20061538 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:20061538 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:20061538 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:20061538 | pubmed:issn | 1522-1539 | lld:pubmed |
| pubmed-article:20061538 | pubmed:author | pubmed-author:JosKK | lld:pubmed |
| pubmed-article:20061538 | pubmed:author | pubmed-author:ChenLuL | lld:pubmed |
| pubmed-article:20061538 | pubmed:author | pubmed-author:WilliamsDavid... | lld:pubmed |
| pubmed-article:20061538 | pubmed:author | pubmed-author:SinghKrishnaK | lld:pubmed |
| pubmed-article:20061538 | pubmed:author | pubmed-author:GaoXiangX | lld:pubmed |
| pubmed-article:20061538 | pubmed:author | pubmed-author:KelleyJimJ | lld:pubmed |
| pubmed-article:20061538 | pubmed:author | pubmed-author:LiChuanfuC | lld:pubmed |
| pubmed-article:20061538 | pubmed:author | pubmed-author:KalbfleischJo... | lld:pubmed |
| pubmed-article:20061538 | pubmed:author | pubmed-author:HuaFangF | lld:pubmed |
| pubmed-article:20061538 | pubmed:author | pubmed-author:HaTuanzhuT | lld:pubmed |
| pubmed-article:20061538 | pubmed:author | pubmed-author:KaoRace LRL | lld:pubmed |
| pubmed-article:20061538 | pubmed:author | pubmed-author:HuYulongY | lld:pubmed |
| pubmed-article:20061538 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:20061538 | pubmed:volume | 298 | lld:pubmed |
| pubmed-article:20061538 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:20061538 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:20061538 | pubmed:pagination | H984-91 | lld:pubmed |
| pubmed-article:20061538 | pubmed:dateRevised | 2011-11-2 | lld:pubmed |
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