Abstract
Background and Aims: Acute liver failure (ALF) is a type of liver injury that is caused by multiple factors and leads to severe liver dysfunction; however, current treatments for ALF are insufficient. Magnesium isoglycyrrhizinate (MgIG), a novel glycyrrhizin extracted from the traditional Chinese medicine licorice, has a significant protective effect against concanavalin A (ConA)-induced liver injury, but its underlying therapeutic mechanism is unclear. Hence, this study aims to explore the potential therapeutic mechanism of MgIG against ConA-induced immune liver injury. Methods: ConA (20 mg/kg, i. v.) was administered for 12 h to construct an immune liver injury model, and the treatment group was given MgIG (30 mg/kg, i. p.) injection 1 h in advance. Lethality, liver injury, cytokine levels, and hepatocyte death were evaluated. The level of autophagy was evaluated by electron microscopy, RT-PCR and western blotting, and hepatocyte death was assessed in vitro by flow cytometry. Results: MgIG significantly increased the survival rate of mice and ameliorated severe liver injury mediated by ConA. The decrease in the number of autophagosomes, downregulation of LC3b expression and upregulation of p62 expression indicated that MgIG significantly inhibited ConA-induced autophagy in the liver. Reactivation of autophagy by rapamycin (RAPA) reversed the protective effect of MgIG against ConA-induced liver injury. Compared with MgIG treatment, activation of autophagy by RAPA also promoted the expression of liver inflammation markers (IL-1β, IL-6, TNF-α, CXCL-1, CXCL-2, CXCL-10, etc.) and hepatocyte death. In vitro experiments also showed that MgIG reduced ConA-induced hepatocyte death but did not decrease hepatocyte apoptosis by inhibiting autophagy. Conclusion: MgIG significantly ameliorated ConA-induced immune liver injury in mice by inhibiting autophagy. This study provides theoretical support for the ability of MgIG to protect against liver injury in clinical practice.
Highlights
Acute liver failure (ALF) is a severe form of liver dysfunction characterized by abnormal liver biochemical indicators, jaundice, and coagulation dysfunction as the main clinical manifestations, and approximately half of the patients experience multiple organ failure and death; ALF imposes a heavy burden on society (Wendon et al, 2017; Weiler et al, 2020)
The results showed that Magnesium isoglycyrrhizinate (MgIG) significantly ameliorated acute liver injury in mice
hematoxylin and eosin (H&E) staining of liver tissue sections showed that the liver tissue in the concanavalin A (ConA) model group was severely congested and showed large necrotic areas, while liver injury in the MgIG treatment group was significantly reduced (Figure 1D)
Summary
Acute liver failure (ALF) is a severe form of liver dysfunction characterized by abnormal liver biochemical indicators, jaundice, and coagulation dysfunction as the main clinical manifestations, and approximately half of the patients experience multiple organ failure and death; ALF imposes a heavy burden on society (Wendon et al, 2017; Weiler et al, 2020). As a novel glycyrrhizic acid extracted from the traditional Chinese medicine licorice, MgIG has anti-inflammatory, antioxidant, antiviral, immunoregulatory and hepatocellular protective effects (Tang et al, 2021). There has been little research on the mechanism underlying the effect of MgIG against concanavalin A (ConA)induced immune liver injury. Acute liver failure (ALF) is a type of liver injury that is caused by multiple factors and leads to severe liver dysfunction; current treatments for ALF are insufficient. Magnesium isoglycyrrhizinate (MgIG), a novel glycyrrhizin extracted from the traditional Chinese medicine licorice, has a significant protective effect against concanavalin A (ConA)-induced liver injury, but its underlying therapeutic mechanism is unclear. This study aims to explore the potential therapeutic mechanism of MgIG against ConA-induced immune liver injury
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