No abstract

Colchicine and albendazole inhibited LPS-induced secretion of TNF-α and NO in a primary culture of rat Kupffer cells. Both agents potentiated the stimulating effect of this toxin on prostaglandin E2 secretion. The amount of prostaglandin D2 remained unchanged under these conditions.

Low doses (0.143 pg/ml per 1cP cells) of the lipopolysaccharide toxin (LPS) from Sulmonellu typhimurium were shown to increase (after an 18 h incubation) the intracellular content of free cholesterol (CH), esterified cholesterol (EC) and triglycerides (TG) by 3040% in the primary culture of rabbit hepatocytes. A similar increase was found for the incorporation of r4C]acetate into these lipids. The concentration of lipids in cultural medium, under these conditions, was also augmented: by 30-40s for CH; by 5&60% for TG and by 6&80% for EC. Higher doses (up to 50 ,ug/ml) of LPS hardly affected the lipid content in hepatocytes but strongly (by two-fold) inhibited the secretion of lipids. It is suggested that in vivo low concentrations of LPS in bloodstream (in the absence of conspicuous pathology) might induce hyperlipidemia directly influencing on hepatic cells, while, under the higher concentrations of LPS, hyperlipidemia caused by cachectin (or tumor necrosis factor) is probably observed.Lipopolysaccharide toxin; Hyperlipidemia; (Rabbit hepatocyte)

Ivermectin had no effect on phagocytic function of liver macrophages, but blocked LPS-induced secretion of tumor necrosis factor, NO, prostaglandin E2, and increase of intracellular concentration of Ca2+. These inhibitory effects were observed only in the presence of chlorine ions in the extracellular medium, which attested to involvement of glycine-dependent chlorine channels.