ArticleDrug design, development and therapy2016
Amelioration of concanavalin A-induced autoimmune hepatitis by magnesium isoglycyrrhizinate through inhibition of CD4(+)CD25(-)CD69(+) subset proliferation.
Article in Drug design, development and therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 39 citations in OpenAlex.
- Single chiral center epimerization-modulated multi-carrier-free oral hydrogel for remolding inflammatory microenvironment via PI3K/Akt/NF-κB and MAPK signaling pathways.Bioactive materials · 2026Article
- Exosome-Modified AAV Gene Therapy Attenuates Autoimmune Hepatitis via Enhanced Regulatory T Cell Targeting and Immune Modulation.Microorganisms · 2025Article
- Magnesium isoglycyrrhizinate prevented the liver injury of acetaminophen by promoting mitochondrial biogenesis.Toxicology research · 2025Article
- Glycosides as Potential Medicinal Components for Ulcerative Colitis: A Review.Molecules (Basel, Switzerland) · 2023Review
- MgIG Attenuates Oxaliplatin-induced Hepatotoxicity through Suppression of Connexin 43 in Hepatic Stellate Cells.Journal of clinical and translational hepatology · 2023Article
- NLRP3 inflammasome activation in response to metals.Frontiers in immunology · 2023Review
- Magnesium isoglycyrrhizinate attenuates acute alcohol-induced hepatic steatosis in a zebrafish model by regulating lipid metabolism and ER stress.Nutrition & metabolism · 2022Article
- Jiegeng Decoction Potentiates the Anticancer Efficacy of PaclitaxelFrontiers in pharmacology · 2022Article
- Summary of Natural Products Ameliorate Concanavalin A-Induced Liver Injury: Structures, Sources, Pharmacological Effects, and Mechanisms of Action.Plants (Basel, Switzerland) · 2021Review
- Novel Therapies for the Treatment of Drug-Induced Liver Injury: A Systematic Review.Frontiers in pharmacology · 2021Review
- Human liver stem cells attenuate concanavalin A-induced acute liver injury by modulating myeloid-derived suppressor cells and CD4Stem cell research & therapy · 2019Article
- Protective Effects of Magnesium Glycyrrhizinate on Methotrexate-Induced Hepatotoxicity and Intestinal Toxicity May Be by Reducing COX-2.Frontiers in pharmacology · 2019Article
- Anti-CD69 therapy induces rapid mobilization and high proliferation of HSPCs through S1P and mTOR.Leukemia · 2018Article
- Magnesium isoglycyrrhizinate ameliorates doxorubicin-induced acute cardiac and hepatic toxicity via anti-oxidant and anti-apoptotic mechanisms in mice.Experimental and therapeutic medicine · 2018Article
- Amelioration of Ethanol-Induced Hepatitis by Magnesium Isoglycyrrhizinate through Inhibition of Neutrophil Cell Infiltration and Oxidative Damage.Mediators of inflammation · 2017Article
- miR-20b Inhibits T Cell Proliferation and Activation via NFAT Signaling Pathway in Thymoma-Associated Myasthenia Gravis.BioMed research international · 2016Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Magnesium isoglycyrrhizinate (MGL) is a new stereoisomer of glycyrrhizic acid, which is clinically used as a hepatoprotective medicine with more potent effects and less side effects than glycyrrhizic acid. This study was designed to evaluate the protective effects and possible mechanism of MGL against concanavalin A (Con A)-induced autoimmune hepatitis. Hepatitis was induced by Con A in C57/6J mice with or without MGL administration; injury score and serum ALT were evaluated. The CD4(+) T-cells were isolated from splenocytes and challenged with Con A after coculturing with MGL. The injury score was significantly improved in MGL-treated mice after Con A challenging for 12 and 24 hours compared with those merely challenged with Con A. Similar trends were observed in the serum levels of ALT and AST. The most interesting result was that MGL administration significantly decreased the frequency of CD4(+)CD25(-)CD69(+) T-cells rather than CD4(+)CD25(+)CD69(+) T-cells in peripheral blood mononuclear cells, after Con A challenging 12 and 24 hours. Moreover, the serum ALT levels were markedly correlated with the frequency of CD4(+)CD25(-)CD69(+) cells, but only weakly correlated with CD4(+)CD25(+)CD69(+) cells in peripheral blood mononuclear cells. More importantly, MGL (5 mg/mL) almost completely eliminated the proliferation of the CD25(-)CD69(+) subset in primary CD4(+) T-cells after Con A challenge. Compared with merely Con A-challenged mice, those with MGL administration significantly demonstrated decreased NALP3, NLRP6, and caspase-3 expression, in which the NALP3 and caspase-3 downregulated in a dose-dependent manner. Our results indicate that MGL may have potential as a therapeutic agent in autoimmune hepatitis by ameliorating liver injury. Its molecular mechanism may be involved in inhibiting CD4(+)CD25(-)CD69(+) subset proliferation and downregulating inflammasome expression in liver tissue.
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