Ginsenoside F1 Attenuates Eosinophilic Inflammation in Chronic Rhinosinusitis by Promoting NK Cell Function
- Background: Ginsenosides have beneficial effects on several airway inflammatory disorders primarily
through glucocorticosteroid-like anti-inflammatory activity. Among inflammatory cells, eosinophils play
a major pathogenic role in conferring a risk of severe refractory diseases including chronic rhinosinusitis
(CRS). However, the role of ginsenosides in reducing eosinophilic inflammation and CRS pathogenesis is
Methods: We investigated the therapeutic efficacy and underlying mechanism of ginsenoside F1 (G-F1)
in comparison with those of dexamethasone, a representative glucocorticosteroid, in a murine model of
CRS. The effects of G-F1 or dexamethasone on sinonasal abnormalities and infiltration of eosinophils and
mast cells were evaluated by histological analyses. The changes in inflammatory cytokine levels in
sinonasal tissues, macrophages, and NK cells were assessed by qPCR, ELISA, and immunohistochemistry.
Results: We found that G-F1 significantly attenuated eosinophilic inflammation, mast cell infiltration,
epithelial hyperplasia, and mucosal thickening in the sinonasal mucosa of CRS mice. Moreover, G-F1
reduced the expression of IL-4 and IL-13, as well as hematopoietic prostaglandin D synthase required for
prostaglandin D2 production. This therapeutic efficacy was associated with increased NK cell function,
without suppression of macrophage inflammatory responses. In comparison, dexamethasone potently
suppressed macrophage activation. NK cell depletion nullified the therapeutic effects of G-F1, but not
dexamethasone, in CRS mice, supporting a causal link between G-F1 and NK cell activity.
Conclusion: Our results suggest that potentiating NK cell activity, for example with G-F1, is a promising
strategy for resolving eosinophilic inflammation in CRS.
- 김소정; 이진주; 최우선; 김효정; 김미연; 김선창; 김헌식
- Issued Date
- Ginsenoside; F1; NK cell; Chronic rhinosinusitis; Eosinophilic inflammation
- Journal of Ginseng Research
- Citation Volume
- Citation Number
- Citation Start Page
- Citation End Page
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