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Role of peroxisome proliferator-activated receptors δ (PPARδ) in rats showing endotoxemic heart failure
Ping-Chin Chang, Li-Jen Chen, Juei-Tang Cheng
Jazyk angličtina Země Česko
Typ dokumentu práce podpořená grantem
- Klíčová slova
- GW0742,
- MeSH
- endotoxemie * farmakoterapie MeSH
- hemodynamika účinky léků MeSH
- intracelulární "calcium-sensing" proteiny MeSH
- kardiomyocyty metabolismus patologie účinky léků MeSH
- kontrakce myokardu účinky léků MeSH
- krevní tlak účinky léků MeSH
- krysa rodu rattus MeSH
- kultivační techniky MeSH
- lipopolysacharidy * aplikace a dávkování MeSH
- novorozená zvířata MeSH
- potkani Wistar MeSH
- receptory aktivované proliferátory peroxizomů * účinky léků MeSH
- srdeční selhání * patologie MeSH
- statistika jako téma MeSH
- thiazoly aplikace a dávkování MeSH
- troponin I metabolismus MeSH
- western blotting MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- práce podpořená grantem MeSH
PPARδ-dependent maintenance of inotropic function is mentioned as crucial for cardiomyocytes. However, change of PPARδ in endotoxins-induced cardiac dysfunction is still unclear. The present study is then designed to investigate the changes of PPARδ in rats showing LPS-induced cardiac dysfunction. In the in vivo experiments, adult Wistar rats were treated with intravenous injection of 10 mg/kg LPS for 6 h. The isolated heart determined in Langendorff apparatus and the hemodynamic analysis of rats used to measure the changes of cardiac function extra vivo and in vivo. We found that LPS decreased the cardiac contractility in isolated heart and lowered the hemodynamic dP/dtmax in rats. Also, this action of LPS was reversed by PPARδ agonist. In cultured neonatal rat cardiac cells incubated with LPS, the intracellular calcium concentration and troponin I phosphorylation were both reduced after the detection of intracellular calcium level and Western blotting analysis. PPARδ agonist also reversed both actions of LPS in cardiomyocyte. The obtained results suggest that LPS induced decreases in PPARδ expression and troponin I phosphorylation to result in acute heart failure similar to cardiac dysfunction in endotoxemia.
Department of Infection Chi Mei Medical Center Liouying Liou Ying Tainan City Taiwan
Department of Medical Research Chi Mei Medical Center Yong Kang City Tiwan
Citace poskytuje Crossref.org
Literatura
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