Abstract
Abstract Objective The aim of this study was to investigate the effect of Thalidomide and Etanercept on inflammation parameters in a neonatal rat sepsis model induced with Lipopolysaccharide (LPS). Materials and methods Four-week-old male Wistar Albino rats were used in the experiment. LPS (5 mg/kg) was administered to rats as sepsis-inducing agent and two anti-inflammatory drugs, Thalidomide and Etanercept were given intraperitoneally as chemotherapeutic agents. The septic neonatal rats were treated with Thalidomide (0.5 mg/kg), Etanercept (1 mg/kg), and a combination of the two. All therapeutic agents were injected half an hour after injecting LPS. It took 24 h to perform the entire experiment. Whereupon, liver tissues of the animals were removed, presepsin of liver tissue and NF-κB levels were measured by ELISA analysis and NF-κB protein expression levels were determined by Western blotting. Results A significant increase was detected in presepsin and NF-κB levels in LPS group compared to sham and treatment groups. In Western Blot evaluations, there was a significant decrease in the expression of NF-κB protein in treatment groups compared to sepsis group. Conclusions It was observed that Thalidomide and Etanercept had potential effects on the treatment of neonatal sepsis.
Highlights
Affecting multiple bodily systems, neonatal sepsis is a serious condition with a high mortality rate and leads to hemodynamic changes as shock, organ dysfunction, and organ failure
The aim of this study was to investigate the effect of Thalidomide and Etanercept on inflammation parameters in a neonatal rat sepsis model induced with Lipopolysaccharide (LPS)
It was observed that Thalidomide and Etanercept had potential effects on the treatment of neonatal sepsis
Summary
Neonatal sepsis is a serious condition with a high mortality rate and leads to hemodynamic changes as shock, organ dysfunction, and organ failure. When LPS is injected to the body, defense cells trigger a series of inflammatory responses, including forming a LPS-LPB-CD14 complex, which is made up of LPS, LPS-binding proteins (LPB), alongside forming CD14 glycoprotein, which serves as a specific receptor task for LPS and LPB. This complex activates the inflammatory cascade, upon which monocytes and macrophages cause the release of proinflammatory cytokines and interleukins. This subtype contributes to the transmission of intracellular signals, playing an important role in the occurrence of septic shock [5, 6]
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