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Updated: Jan 20, 2026
Intravital Microscopy of Leukocyte-endothelial and Platelet-leukocyte Interactions in Mesenterial Veins in Mice
Published on: August 13, 2015
Ginsenoside Rg3-enriched red ginseng extract mitigates sepsis by inhibiting platelet-leukocyte aggregates and
Yuan Yee Lee1, Abdul Wahab Akram1, Evelyn Saba2
1Department of Veterinary Medicine, College of Veterinary Medicine, Kyungpook National University, Daegu, 41566, Republic of Korea.
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 in vivo effects of Rg3-RGE were analyzed in a lipopolysaccharide (LPS)-induced murine model of sepsis. Flow cytometry was used to evaluate platelet-leukocyte activation markers. Confocal and scanning electron microscopy (SEM) provided visual evidence of aggregate formation. ELISA was used to quantify plasma levels of tissue factor (TF) and platelet factor 4 (PF4). HPLC analysis revealed the presence of Rb1, Rg3 [20(S) and 20(R)], Rc, Rd, Rf, Rh1, Rb2, and Rg2 [20(S)] in Rg3-RGE. Network pharmacology was employed to identify target interactions and assess their involvement in the thrombo-inflammatory pathway.
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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