Magnesium isoglycyrrhizinate attenuates D-galactosamine/lipopolysaccharides induced acute liver injury of rat via regulation of the p38-MAPK and NF-κB signaling pathways

Context: Acute hepatic failure involves in serious inflammatory responses and leads to a high mortality. Magnesium isoglycyrrhizinate (MgIG), a magnesium salt of 18-alpha glycyrrhizic acid (GA) stereoisomer, has been shown anti-inflammatory activity previously. Objective: This study aimed to investigate the protective effects of MgIG, a hepatocyte protective agent, on D-galactosamine and lipopolysaccharide (D-GalN/LPS)-induced acute liver injury in rats, and meanwhile explore the molecular mechanism. Materials and methods: Male Sprague-Dawley (SD) rats were injected with D-GalN/LPS (800 mg/kgBW/10 mu g/kgBW) with or without administration of MgIG (225 mg/kg once 6 h after D-GalN/LPS injection and MgIG 45 mg/kg twice in another 12 h, intraperitoneal injection). Rats were sacrificed 24 h after D-GalN/LPS injection, the blood and liver samples were collected for future inflammation and hepatotoxicity analyses. Results: MgIG significantly inhibited D-GalN/LPS-induced inflammatory cytokines production and hepatotoxicity as indicated by both diagnostic indicators of liver damage [aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels] and histopathological analysis. Western blot analysis demonstrated that MgIG significantly decreased p38-mitogen activated protein kinase (MAPK) and nuclear factor kappa B (NF-kappa B) activation induced by D-GalN/LPS. Conclusion: The results indicated that the protective effects of MgIG on D-GalN/LPS-induced acute liver injury might be correlated with its capacity to regulate the p38-MAPK and NF-kappa B signaling pathways.