NDLI: Inhibition effect of glycyrrhizin in lipopolysaccharide-induced high-mobility group box 1 releasing and expression from RAW264.7 cells.

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Inhibition effect of glycyrrhizin in lipopolysaccharide-induced high-mobility group box 1 releasing and expression from RAW264.7 cells.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Wu, Chuan-Xin He, Lin-Xiang Guo, Hui Tian, Xiao-Xing Liu, Qi Sun, Hang
Description	Country affiliation: China Author Affiliation: Wu CX ( *Department of Hepatobiliary Surgery and Institute for Viral Hepatitis, Key Laboratory of Molecular Biology for Infectious Diseases, Ministry of Education, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.)
Abstract	INTRODUCTION: High-mobility group box 1 (HMGB1) is a therapeutic target for sepsis. Glycyrrhizin (GL) is the aglycone of glycyrrhizin derived from licorice. We clarified the anti-inflammatory effects of GL. We explored the anti-HMGB1 effect of GL and elucidated its molecular mechanism, which will be of benefit for sepsis treatment. METHODS: We stimulated murine macrophage-like RAW 264.7 cells with lipopolysaccharide (LPS) and LPS + GL, then measured the expression and release of HMGB1. The expression of related signal transduction factors was detected. RESULTS: High-mobility group box 1 was distributed mainly in the nucleus with lower cytoplasmic levels in RAW 264.7 cells before LPS stimulation. After stimulation, cytoplasmic HMGB1 levels increased gradually, whereas in nuclear fluctuation a trend of HMGB1 expression was observed. Significant upregulation of HMGB1 mRNA occurred 12 h after LPS stimulation. Glycyrrhizin prevented the transfer of HMGB1 from the nucleus to the cytoplasm and inhibited upregulation of HMGB1 mRNA induced by LPS. Phospho-p38 mitogen-activated protein kinase and activated activating protein 1 increased significantly 8 h after LPS stimulation. Tumor necrosis factor and interleukin 6 increased 4 h after LPS stimulation and peaked at 48 h, and HMGB1 increased at 8 h. The Toll-like receptor 4/MD2/nuclear factor κB signaling pathway was activated 4 h after LPS stimulation. Glycyrrhizin inhibited this pathway. CONCLUSIONS: Glycyrrhizin inhibited the expression and release of HMGB1 through blocking the p38 mitogen-activated protein kinase/activating protein 1 signaling pathway then inhibited the massive release of tumor necrosis factor and interleukin 6.
File Format	HTM / HTML
ISSN	10732322
Issue Number	4
Volume Number	43
e-ISSN	15400514
Journal	Shock
Language	English
Publisher	Lippincott Williams & Wilkins
Publisher Date	2015-04-01
Publisher Place	United States
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Intensive care medicine Glycyrrhizic Acid Chemistry Hmgb1 Protein Metabolism Lipopolysaccharides Sepsis Drug Therapy Animals Anti-inflammatory Agents Cell Nucleus Cytoplasm Inflammation Interleukin-6 Mice Microscopy, Fluorescence Raw 264.7 Cells Signal Transduction Tumor Necrosis Factor-alpha P38 Mitogen-activated Protein Kinases Journal Article Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Emergency Medicine Critical Care and Intensive Care Medicine

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Inhibition effect of glycyrrhizin in lipopolysaccharide-induced high-mobility group box 1 releasing and expression from RAW264.7 cells.