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

Abstract

Context: Acute hepatic failure involves in serious inflammatory responses and leads to a high mortality. Magnesium isoglycyrrhizinate (MgIG), a magnesium salt of 18-α 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-GaIN/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-GaIN/LPS (800 mg/kgBW/10 μg/kgBW) with or without administration of MgIG (225 mg/kg once 6 h after D-GaIN/LPS injection and MgIG 45 mg/kg twice in another 12 h, intraperitoneal injection). Rats were sacrificed 24 h after D-GaIN/LPS injection, the blood and liver samples were collected for future inflammation and hepatotoxicity analyses.

Results: MgIG significantly inhibited D-GaIN/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-κB) activation induced by D-GaIN/LPS.

Conclusion: The results indicated that the protective effects of MgIG on D-GaIN/LPS-induced acute liver injury might be correlated with its capacity to regulate the p38-MAPK and NF-κB signaling pathways.

Keywords:

• Magnesium isoglycyrrhizinate
• D-GalN/LPS
• acute liver injury
• p38- MAPK
• NF-κB

Disclosure statement

No potential conflict of interest was reported by the authors.

Additional information

Funding

The authors wish to thank the Foundation of Peking University Third Hospital and Foundation of Beijing Haidian Preventive Medicine Association [No. 2017HDPMA03] for the funding of this work.