Hydroxyethyl Starch 130/0.4 Inhibits Production of Plasma Proinflammatory Cytokines and Attenuates Nuclear Factor-κB Activation and Toll-Like Receptors Expression in Monocytes During Sepsis

BackgroundHydroxyethyl starch (HES) is one of the most frequently used plasma substitutes, and could modulate inflammatory response in sepsis. Our aim of this study was to investigate the mechanism of the effect of HES 130/0.4 by studying plasma levels of inflammatory cytokines, nuclear factor-κB (NF-κB) activation, and Toll-like receptors (TLRs) expression in peripheral monocytes during polymicrobial sepsis.Materials and MethodsRats with sepsis induced by cecal ligation and puncture (CLP) were treated with HES130/0.4 (7.5, 15, or 30 mL/kg, intravenously); then, rat plasma and monocytes were isolated from blood 5 h later. The plasma level of cytokines (tumor necrosis factor [TNF]-α and interleukin [IL]-6), NF-κB activity, and mRNA and protein levels of TLRs (TLR2 and TLR4) in peripheral blood monocytes were determined by enzyme-linked immunosorbent assay, electrophoretic mobility shift assay, reverse transcription-polymerase chain reaction, and Western blotting, respectively.ResultsHES130/0.4 dose-dependently reduced the plasma level of TNF-α and IL-6 in rats with sepsis. HES130/0.4 also significantly inhibited NF-κB activation, and TLRs mRNA and protein levels in peripheral monocytes.ConclusionDuring sepsis, HES130/0.4 can down-regulate the inflammatory response, possibly through inhibition of the TLRs/NF-κB signaling pathway, and could be one more appropriate plasma substitute in sepsis.