LPS exerts time- and dose-dependent effects on cellular function in H9c2 cells. LPS is known to induce cardiac hypertrophy and apoptosis in the heart. We treated H9c2 cells with LPS at various concentrations for two different exposure times. First, H9c2 cells were incubated with 1, 5, and 10 μg/ml LPS for 3 h.

2024年10月17日 · Heart mass indexed to body mass in the LPS group was significantly higher compared to the control group (P = 0.002). The internal diameter of the LV chamber during both diastole (P = 0.04) and...

2017年6月7日 · Our data demonstrate that hiPSC-CMs possess the functional reaction system involved in endotoxin-induced inflammation and can model some bacterium-induced inflammatory responses in cardiac...

2022年1月25日 · In this study, we investigate the effect of LPS on NE production in ICA cells and the role of ICA cell-derived NE in LPS-induced myocardial dysfunction.

1997年12月19日 · We hypothesized that LPS, in clinically relevant levels (1 ng/mL), directly depresses contractility and β-adrenergic responses in cardiac myocytes. Cardiac myocytes were isolated from the left ventricle of adult rabbits using digestive enzymes (collagenase and …

2024年9月24日 · LPS pretreatment confers cardiac protection against ISO-induced injury through TLR4 mediated type 1 and 2 interferon signaling, consistent with trained innate immune tolerance.

2001年3月16日 · Fluorescently labeled LPS was used to treat primary cardiomyocyte cultures, perfused heart preparations, and the RAW264.7 macrophage cell line. Using confocal microscopy and spectrofluorometry, we found that LPS was rapidly internalized in cardiomyocyte cultures and Langendorff-perfused hearts.

2019年8月2日 · 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.

2023年12月20日 · We demonstrated that ALDH2 alleviated LPS-induced cardiac dysfunction, inflammation, and apoptosis through the cGAS/STING signaling pathway, thereby protecting against LPS-induced cardiac injury. This study identifies a novel therapeutic approach for treating sepsis-induced cardiomyopathy (SIC).

The presented results showed that rutin significantly improved morphological changes of myocardium and relieved cardiac marker enzymes [creatine kinase (CK) and lactate dehydrogenase (LDH)] level to protect heart in LPS-induced sepsis.