Red ginseng extract inhibits lipopolysaccharide-induced platelet-leukocyte aggregates in mice

• Published in: Journal of ginseng research Vol. 48; no. 4; pp. 428 - 434
• Main Authors: Yuan Yee Lee, Sung Dae Kim, Jin-Kyu Park, Won-Jae Lee, Jee Eun Han, Min-Soo Seo, Min-Goo Seo, Seulgi Bae, Dongmi Kwak, Evelyn Saba, Man Hee Rhee
• Format: Journal Article
• Language: Korean
• Published: 2024
• Subjects: Red ginseng extract; Platelet activation; Inflammation; Platelet-leukocyte aggregates; Thrombosis
• ISSN: 1226-8453; 2093-4947

Background: Platelet-leukocyte aggregates (PLAs) play important roles in cardiovascular disease and sepsis. Red ginseng extract (RGE) has been well-studied for its antiplatelet and anti-inflammatory activities. However, the potential inhibitory effects of RGE on PLA have not been investigated. Methods: Six-week-old ICR mice were given oral gavage of RGE for 7 days, followed by an intraperitoneal injection of 15 mg/kg of lipopolysaccharide. Mice were euthanized 24 h later, and blood samples were collected for further analysis. Flow cytometry was utilized to sort populations of PLAs and platelet-neutrophil aggregates (PNAs). By using confocal microscopy, PNAs were validated. Morphological changes in platelets and leukocytes were visualized with scanning electron microscopy. Expressions of tissue factor (TF) and platelet factor 4 (PF4) were investigated using enzyme-linked immunosorbent assay. Results: Populations of activated platelets, PLAs and PNAs, were significantly increased with LPS-induction. Treatment with 200 and 400 mg/kg of RGE decreased platelet activation. Moreover, the populations of PLAs and PNAs were reduced. PNAs were visible in the blood of septic mice, and this was attenuated by treatment with 400 mg/kg of RGE. Morphologically, sepsisinduced platelet activation and fibrin formation in the blood. This was reduced with RGE treatment. Sepsis-induced increase in the plasma levels of TF and PF4 was also reduced with RGE treatment. Conclusion: This study shows that RGE is a potential therapeutic that reduces the activation of platelets and targets PLA and PNA formation. Detailed inhibitory mechanisms of RGE should be studied.