ArticleAmerican journal of translational research2024
Glycyrrhizin inhibits LPS-induced neutrophil-like release of NETs.
Article in American journal of translational research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Spatiotemporal heterogeneity of neutrophil extracellular traps in hepatocellular carcinoma microenvironment and targeted therapy progress.Journal of translational medicine · 2026Review
- Targeting the Toll-Like Receptor 4 Ameliorates Heart Failure in Aged Mice by Inhibiting the Formation of Neutrophil Extracellular Traps.Physiological research · 2026Article
- Catalpol mitigates rheumatoid arthritis by targeting neutrophil extracellular trap release.Frontiers in immunology · 2026Article
- Liver ischemia-reperfusion promotes tumor metastasis via neutrophil-endothelial interactions: targeting ICAM1 to prevent metastatic recurrence.Journal of translational medicine · 2025Article
- Neutrophil/monocyte-targeted dual-ligands modified liposomes delivering puerarin for ischemia stroke treatment.Materials today. Bio · 2025Article
- A Direct Relationship Between 'Blood Stasis' and Fibrinaloid Microclots in Chronic, Inflammatory, and Vascular Diseases, and Some Traditional Natural Products Approaches to Treatment.Pharmaceuticals (Basel, Switzerland) · 2025Review
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Authors and funding
8 authors.
Funding
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Abstract
objectiveTo investigate the regulatory effect of glycyrrhizin (GL) on the release of neutrophil extracellular traps (NETs) from neutrophils in sepsis.
methodsHL-60 cells were induced to differentiate into neutrophil-like dHL-60 cells to establish a neutrophil-like sepsis model. Expression levels of high-mobility group box 1 (HMGB1), citrullinated histone H3 (Cit-H3), and Toll-like receptor 9 (TLR9) were assessed by Western blotting. Free DNA, a component of NETs, was quantified using a fluorescence microplate reader. Cellular immunofluorescence analysis was used to detect the expression of the key NETs protein, Cit-H3.
resultsdHL-60 cells stimulated with 200 ng/ml LPS exhibited the highest expression of Cit-H3. The neutrophil-like sepsis model showed significantly increased levels of Cit-H3 and HMGB1. GL intervention significantly reduced the expression levels of HMGB1 and Cit-H3 and decreased the free DNA level. These findings suggest that GL decreases HMGB1 expression and NET release in the neutrophil-like sepsis model. TLR9 expression was significantly elevated in the sepsis model. Exogenous recombinant human HMGB1 protein further increased TLR9 expression, while GL inhibited this increase.
conclusionGL may inhibit NET release in sepsis through the HMGB1/TLR9 pathway.
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