4.7 Article

Ursolic acid inhibits FceRI-mediated mast cell activation and allergic inflammation

Journal

INTERNATIONAL IMMUNOPHARMACOLOGY
Volume 99, Issue -, Pages -

Publisher

ELSEVIER
DOI: 10.1016/j.intimp.2021.107994

Keywords

Mast cell; Ursolic acid; Allergic inflammation; Histamine

Funding

  1. National Research Foundation of Korea - Korean government [2019R1C1C1005172, 2019M3A9H1103690, 2020R1A2C1010962, 2017M3A9G8083382, 2020M3A9D3038894]
  2. National Research Foundation of Korea [2019M3A9H1103690, 2020M3A9D3038894, 2020R1A2C1010962, 2019R1C1C1005172] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

Ask authors/readers for more resources

The study demonstrated that ursolic acid (UA) exerts anti-allergic effects by inhibiting FceRI-mediated mast cell activation. It suppresses mast cell degranulation by reducing intracellular calcium levels and inhibits the expression and release of inflammatory cytokines. Furthermore, UA also inhibits passive cutaneous anaphylaxis and active systemic anaphylaxis reactions in a mouse model in a dose-dependent manner.
Background: Mast cells are the primary cells that play a crucial role in the allergic diseases via secretion of diverse allergic mediators. Ursolic acid (UA) is a naturally occurring anti-inflammatory triterpenoid possessing various biological properties such as immune regulation, antioxidant, and anti-fibrotic. The aim of this study was to evaluate the effects of UA in FceRI-mediated mast cell activation and allergic inflammation. Methods: In this study, mast cells were stimulated with immunoglobulin E (IgE) and the anti-allergic effects of UA were assessed by measuring the levels of allergic mediators. In vivo effects of UA were observed by generating passive cutaneous anaphylaxis (PCA) and active systemic anaphylaxis (ASA) in mouse model. Results: We found that UA inhibited the degranulation of mast cell by suppressing the intracellular calcium level in a concentration-dependent manner. UA inhibited the expression and the release of pro-inflammatory cytokines in mast cells. Anti-allergic effects of UA were demonstrated via suppression of FceRI-mediated signaling mole-cules. In addition, UA inhibited the IgE-mediated PCA and ovalbumin-induced ASA reactions in a dose-dependent manner. Conclusions: Based on these findings, we suggest that UA might have potential as a therapeutic candidate for the treatment of allergic inflammatory diseases via inhibition of FceRI-mediated mast cell activation.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.7
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available