Role of peroxisome proliferator-activated receptors δ (PPARδ) in rats showing endotoxemic heart failure

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 contrac-tility in isolated heart and lowered the hemodynamic dp/dtmax in rats. also,this action of lps was reversed by ppard 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. © 2013 faculty of health and social studies,university of south bohemia in ceske budejovice. published by elsevier urban & partner sp. z o.o. all rights reserved.