The direct effect of lipopolysaccharide on an isolated heart is different from the effect on cardiac myocytes in vitro

Abstract

Introduction: Lipopolysaccharide (LPS) is widely used to induce experimental animals. However, its effects on cardiac contraction is controversial. Although LPS probably induces its influence in vivo both directly and indirectly, we focused on the direct effects of LPS in this report. Material and methods: Isolated ventricular myocytes mounted on a Langendorff apparatus were perfused with LPS. The changes in cultured H9c2 cells incubated with LPS over a 3-h exposure were compared with the changes after a 24-h incubation. Apoptosis was identified using flow cytometry and Western blotting. The mRNA levels were also determined. Results: LPS directly stimulated cardiac contractility at low doses, although it produced inhibition at higher doses. The TLR4-coupled JAK2/STAT3 pathway was identified in H9c2 cells after LPS treatment, with an increase in intracellular calcium levels. LPS dose-dependently activated hypertrophic signals in H9c2 cells and induced apoptosis at the high dose. However, apoptosis was observed in H9c2 cells after a 24-h exposure to LPS, even at low doses. This observation appears to be associated with the level of paracrine cytokines. Changes in H9c2 cells by LPS were diminished by NPS2390, an inhibitor of the calcium-sensing receptor (CaSR). LPS also promoted CaSR mRNA expression in H9c2 cells, which may be unrelated to the changes in cytokine expression influenced by an inflammasome inhibitor. Conclusions: In contrast to the isolated hearts, LPS activated hypertrophic signals prior to apoptotic signals in cardiac cells. Thus, LPS injury appears to be associated with CaSR, which was not markedly influenced by an inflammasome inhibitor.

Curcumin inhibits lipopolysaccharide-induced proximal renal tubular epithelial cell death by regulating ADAMTS18 methylation and AKT/Notch pathways

“…The purpose of this study was to use LPS to induce a renal inflammatory cell model and then knock down ADAMTS18 to explore the mechanisms underlying its effect on inflammatory factors and renal cell activity. LPS has been intensively used as an effective tool to induce inflammation and thus explore a novel biomarker of the inflammatory response [ 17 , 18 ]. Related studies have reported that PRTECs, as early and important target cells of LPS, can be used to study various renal inflammatory responses [ 19 ].…”