Magnesium isoglycyrrhizinate ameliorates concanavalin A-induced liver injury via the p38 and JNK MAPK pathway

刀豆蛋白A 肝损伤 p38丝裂原活化蛋白激酶 炎症 甘草甜素 促炎细胞因子 医学 药理学 免疫学 细胞凋亡 脂多糖 MAPK/ERK通路 信号转导 生物 体外 生物化学
作者
Yudi Gao,Yuan Tian,Xiangying Zhang,Xiaohui Zhang,Zhongping Duan,Feng Ren,Yu Chen
出处
期刊:Immunopharmacology and Immunotoxicology [Informa]
卷期号:42 (5): 445-455 被引量:15
标识
DOI:10.1080/08923973.2020.1808984
摘要

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.

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