Context

Acute liver failure is a serious disease caused by a variety of factors, and immunological injury is an important pathological process. Comprehensive liver treatment efficacy is poor, and the mortality rate is high. Magnesium isoglycyrrhizinate (MgIG) is a new glycyrrhizin drug extracted from the traditional Chinese medicine licorice. The mechanism by which MgIG regulates ConcanavalinA (ConA)-induced immunological liver injury in mice is not completely clear.

Materials and methods

Immunological liver injury was induced in mice by ConA injection, and the inflammatory macrophages model was induced by lipopolysaccharide (LPS). MgIG was administered 30 min prior to ConA and LPS treatment. The mice in the different groups were sacrificed 12 h after treatment, and macrophages were measured at 30 min, 1 h, and 2 h after induction. Macrophages, liver, and blood samples were then collected for analysis.

Results

After drug administration, the MgIG group showed a marked decrease in serum transaminase levels, reduced apoptosis and hepatic inflammatory responses compared to the ConA group. Furthermore, there was a significant reduction in inflammatory cytokine levels in the serum and liver tissue. In vitro, the expression of inflammatory cytokines was distinctly reduced after MgIG administration. In addition, MgIG pretreatment reduced the expression of inflammatory cytokines and regulated the phosphorylation of p38 and JNK proteins in the MAPK pathway.

Conclusion

These findings demonstrated that MgIG protects against ConA-induced immunological liver injury by markedly alleviating liver inflammation, and this provides guidance for the clinical amelioration of liver inflammation induced by immunological factors.

中文翻译：

---

异甘草酸镁可通过p38和JNK MAPK途径改善伴刀豆球蛋白A引起的肝损伤。

语境

急性肝衰竭是由多种因素引起的严重疾病，免疫损伤是重要的病理过程。肝脏综合治疗效果差，死亡率高。异甘草酸镁（MgIG）是从中药甘草中提取的一种新的甘草甜素药物。MgIG调节小鼠中伴刀豆球蛋白A（ConA）诱导的免疫性肝损伤的机制尚不完全清楚。

材料和方法

通过ConA注射诱导小鼠免疫性肝损伤，并通过脂多糖（LPS）诱导炎性巨噬细胞模型。在ConA和LPS治疗之前30分钟给予MgIG。处理后12小时处死不同组的小鼠，并在诱导后30分钟，1小时和2小时测量巨噬细胞。然后收集巨噬细胞，肝脏和血液样本进行分析。

结果

给药后，与ConA组相比，MgIG组的血清转氨酶水平明显降低，凋亡和肝炎症反应降低。此外，血清和肝组织中的炎性细胞因子水平显着降低。在体外，MgIG给药后炎性细胞因子的表达明显降低。此外，MgIG预处理可降低炎症细胞因子的表达并调节MAPK途径中p38和JNK蛋白的磷酸化。

结论

这些发现表明，MgIG通过显着减轻肝脏炎症来预防ConA诱导的免疫性肝损伤，这为临床改善由免疫学因素诱发的肝脏炎症提供了指导。