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Hydroxyethyl Starch Inhibits NF-B Activation and Prevents the Expression of Inflammatory Mediators in Endotoxic Rats

Address correspondence to Professor Jianguo Xu, Department of Anesthesiology, Jinling Hospital, 305 East Zhongshan Road, Nanjing 210002, P. R. China; tel 86 25 482 7974; fax 86 25 480 8122; e-mail smarttian{at}yahoo.com

Hydroxyethyl starch (HES) has been shown to be beneficial in several inflammatory situations, but the mechanisms are unclear. The present study tested the hypothesis that HES has effects on nuclear factor kappa B (NF-B) activation and the expression of inflammatory mediators induced by lipopolysaccharide. Sepsis was induced in male Wistar rats by injection of lipopolysaccharide (LPS, 6 mg/kg, ip). At 1 min after the LPS challenge, HES was infused via the right external jugular vein at the following doses: 3.75, 7.5, 15, or 30 ml/kg. NF-B activation in peripheral blood mononuclear cells and neutrophils, plasma concentrations of tumor necrosis factor (TNF)-, cytokine-induced neutrophil chemoattractant (CINC), expression of CD11b on the blood neutrophil cell surface, and neutrophil sequestration in multiple organs were examined 2 or 4 hr after the LPS challenge. Treatment of rats with HES (3.75 and 7.5 ml/kg) prevented LPS-induced NF-B activation, and inhibited, in a dose-related manner, LPS-induced TNF- and CINC expression. The 4 graded doses of HES decreased CD11b expression in a dose-dependent manner. HES significantly reduced neutrophil sequestration in lung, heart, and liver. These results suggest that HES has an anti-inflammatory effect in endotoxic rats. This effect is mediated by inhibition in the production pathways for inflammatory mediators, including NF-B activation.

Keywords: hydroxyethyl starch, lipopolysaccharide, NF-B, inflammatory mediators, neutrophils

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