LPS-Induced Changes in Myocardial Markers in Neonatal Rats

Abstract

Lipopolysaccharide (LPS) produces varied systemic metabolic effects. We studied the effects of LPS on the cardiac fatty acid profile and its relationship to energy metabolism and inflammatory mediators that included TNF-α and nitric oxide synthase (NOS) in 10-day-old neonatal rat pups. Rat pups received an i.p. injection of LPS after a 4-hour starvation period, followed by collection of blood and cardiac tissue 4 h following LPS administration. Compared to controls, LPS induced significant hypoglycemia and hyperlactacidemia, suggesting the development of endotoxic shock. The result was a significant depression in total fatty acid levels as well as non-esterified fatty acid in the cardiac tissue of the LPS-treated pups. In addition, LPS-treated pups also showed a significant increase in TNF-α, NOS levels with a depressed redox state and energy metabolism in cardiac tissue. These observations suggest that endotoxic shock in 10-day-old rat pups induces a systemic inflammatory response with a depression in fatty acid metabolism that may contribute to myocardial failure.

Attenuated mRNA expression of lipid metabolism genes in primary hepatocytes following lipopolysaccharide treatment in dairy cows

“…The hexane fraction, rich in FA, inhibited the production of inducible proinflammatory cytokines at the transcriptional level via inactivation of NF-kB (Kim et al, 2013b). Ravindranath et al (2003) found that endotoxic shock in 10-day-old rat pups induced a systemic inflammatory response with a decrease in FA metabolism, which may contribute to myocardial failure. Chen et al (2011) showed that a single dose of LPS significantly increased hepatic triglyceride content and caused hepatic lipid accumulation in mice.…”

Lipopolysaccharides and Prematurity: Effect on the Activity of Respiratory Chain Enzymes in Human Umbilical Venous Endothelial Cells

“…3 In a rat model, LPS induced changes in fatty acid oxidation in cardiac cells, however, the route of LPS application was different. 4 The mechanism of action on energy metabolism of HUVECs is still unknown. PGC-1-related co-activator as an important and essential regulator of mitochondrial function and biogenesis 5 has been shown to be down regulated by LPS in human umbilical venous endothelial cells (HUVEC).…”