Yu Chen

Prof. Dr. Yu Chen

Difficult & Complicated Liver Diseases and Artificial Liver Center & Beijing Municipal Key Laboratory of Liver Failure and Artificial Liver Treatment Research, Beijing YouAn Hospital, Capital Medical University, Beijing, China

Research Focus & Metrics

Academic Career Length

7Years (2020-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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29 August 2020 in Immunopharmacology and Immunotoxicology
Verified
Journal Article
Closed access
YGYudi Gao
Yudi Gao
YTYuan Tian
Yuan Tian
XZXiangying Zhang
Xiangying Zhang
XZXiaohui Zhang
Xiaohui Zhang
ZDZhongping Duan
Zhongping Duan
YCYu Chen
Yu Chen
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 injuryin mice is not completely clear. Objective: 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 ConAand LPS treatment. The mice in the differentgroups were sacrificed 12 h after treatment, and macrophages were measured at 30min, 1h and 2h after induction. Macrophages, liver and blood samples were then collected foranalysis. Results: After drug administration, the MgIG group showed a marked decrease in serumtransaminaselevels, reducedapoptosis and hepatic inflammatory responses compared to the ConA group. Furthermore, there was a significant reduction ininflammatory cytokine levels in the serum and liver tissue.In vitro, the expression of inflammatory cytokines wasdistinctlyreduced 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.