{'fraction_non_alphanumeric': 0.03820086260012323, 'fraction_numerical': 0.013555144793592114, 'mean_word_length': 5.628571428571429, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Suppressive action of resolvin D1 on the production and release of septic mediators in D-galactosamine-sensitized endotoxin shock mice.

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.