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Endotoxin/septic shock is a severe condition induced during serious infections with Gram-negative bacteria. To evaluate the therapeutic potential of resolvin D1 (RvD1), a novel pro-resolving molecule, on endotoxin/septic shock, we investigated the effect of RvD1 on the extracellular release of high mobility group box-1 (HMGB1), the production of inflammatory cytokines, the accumulation of peritoneal cells and hepatocyte apoptosis in vivo using a D-galactosamine (GalN)-sensitized mouse endotoxin shock model. Serum HMGB1 levels were markedly elevated after challenge with lipopolysaccharide (LPS)/D-GalN, and RvD1 administration significantly reduced HMGB1 levels. Furthermore, the serum levels of inflammatory cytokines, such as TNF-α, IL-6, IL-10 and macrophage chemotactic protein (MCP)-1 were elevated in the endotoxin shock model. Importantly, RvD1 administration slightly reduced the TNF-α, IL-6 and IL-10 levels, and further lowered MCP-1 levels. Moreover, RvD1 administration affected the peritoneal cell accumulation and decreased the neutrophil population. Finally, LPS/D-GalN injection induced apoptosis in the liver (mostly of hepatocytes), and RvD1 administration reduced the apoptosis of hepatocytes. These observations suggest that RvD1 may be a therapeutic agent for sepsis/endotoxin shock by exerting suppressive action on the release and production of septic mediators (HMGB1 and inflammatory cytokines), the accumulation of peritoneal cells and hepatic apoptosis.

Suppressive action of resolvin D1 on the production and release of septic mediators in D-galactosamine-sensitized endotoxin shock mice