ArticleToxicology research2025
Magnesium isoglycyrrhizinate prevented the liver injury of acetaminophen by promoting mitochondrial biogenesis.
Article in Toxicology research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Biochemical outcomes and safety profiles of compound glycyrrhizin versus magnesium isoglycyrrhizinate in Kawasaki disease: a retrospective propensity score‑matched cohort study.Translational pediatrics · 2026Article
- The pivotal role of mitochondria in the pathogenesis and treatment of liver failure: a comprehensive review.Molecular and cellular biochemistry · 2026Review
- Precision treatment and frontier advances of glycyrrhizin preparations in drug-induced liver injury (DILI).Frontiers in pharmacology · 2026Review
- Targeting magnesium homeostasis: a novel therapeutic strategy for liver diseases.Frontiers in nutrition · 2026Review
- Glycyrrhizin preparations in liver diseases: a narrative review of mechanisms and therapeutic potential.Frontiers in pharmacology · 2026Review
- Specific Hepatorenal Toxicity and Cross-Species Susceptibility of Eight Representative Pesticides.Toxics · 2025Article
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Authors and funding
12 authors.
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Abstract
Acetaminophen (N-acetyl-para-aminophenol, APAP) is the most widely used antipyretic and anti-inflammatory drug in the world. It is reported that APAP-induced liver damage accounts for about half of all liver failure patients in Europe and the United States. Magnesium isoglycyrrhizinate (MI) is the fourth-generation glycyrrhizic acid preparation developed in China. It has anti-inflammatory, hepatocyte membrane protection, and liver function recovery effects. This study aimed to investigate the effect of MI on alleviating APAP-induced liver injury and explore potential mechanisms. C57 BL/6 J mice were used to assess the efficacy of liver protection, by detecting ALT, AST, H&E and TUNEL staining. Liver samples from saline, APAP, APAP combined with MI group were selected for the transcriptomics analysis. MI significantly prevented the elevation of ALT, and AST. Hepatocyte necrosis was alleviated when MI was co-treated with APAP in TUNEL assay. There were no differences in total GSH levels or GSH/GSSG ration between APAP and MI group. Western Blot MI showed MI didn't affect the protein levels of CYP2E1 expression, mitochondrial p-JNK and cytosolic Endo G. GO analysis showed that mitochondria were the main target of MI in reducing APAP-induced liver injury. MI also significantly upregulated the expression of TFAM, NRF-1, PGC-1β and Sirt1. MI restored mRNA levels of oxidative phosphorylation genes and recovered mitochondrial membrane potential that fell after APAP administration. In conclusion, MI alleviated APAP-induced liver injury by promoting mitochondrial biogenesis.
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