ArticleJournal of ginseng research2026
Ginsenoside Rg3-enriched red ginseng extract mitigates sepsis by inhibiting platelet-leukocyte aggregates and regulates thrombo-inflammatory pathways.
Article in Journal of ginseng research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Ginsenosides fromJournal of ginseng research · 2026Review
- Ginsenoside Rs3 (G-Rs3) inhibits agonist- and oxLDL-mediated platelet activation and attenuatesJournal of ginseng research · 2026Article
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Sepsis is a life-threatening condition characterized by systemic inflammation and thrombo-inflammation, which trigger platelet activation and platelet-leukocyte aggregate (PLA) formation. While Rg3-enriched red ginseng extract (Rg3-RGE) has demonstrated anti-inflammatory and antithrombotic properties, its role in modulating PLAs during sepsis remains poorly understood. Methods: The Results: Rg3-RGE significantly reduced the activated platelets (CD41+CD62P+), platelet-neutrophil aggregates (PNAs; CD41+Ly6G+), and platelet-monocyte aggregates (PMAs; CD41+CD115+). Confocal imaging confirmed a reduction in PNAs. SEM revealed decreased fibrin-like structures and fewer platelet-leukocyte interactions. Rg3-RGE lowered plasma TF levels, indicating a potential effect on the coagulation cascade, though PF4 levels were not significantly altered. Network pharmacology analysis of ginsenosides in Rg3-RGE identified 235 overlapping targets associated with sepsis, inflammation, platelet activation, and PLA formation. Enrichment analysis revealed key thrombo-inflammatory pathways, including platelet activation, MAPK signaling, PI3K-Akt signaling, sphingosine-1-phosphate receptor signaling, and EGFR signaling. Conclusion: Rg3-RGE effectively inhibits platelet-leukocyte aggregate formation and mitigates sepsis-induced platelet-leukocyte interactions.
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Registered trials
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