Abstract
Licochalcone (LicA) is a flavonoid commonly derived from the licorice plant that is reported to have a variety of pharmacological activities. However, few studies have focused on its anti-allergic properties. IgE-mediated passive and systemic anaphylaxis mice models were used to assess the in vivo anti-allergic effect of LicA and its underlying mechanism, while degranulation, cytokines, and chemokines released from laboratory of allergic disease (LAD2) cells were used to assess its in vitro anti-allergic effect. We used western blot analysis to explore the downstream signaling pathway of its anti-allergic effect. We found that in the mouse model, LicA attenuated IgE-mediated paw inflammation, recovered the allergy-induced drop in body temperature, and reduced the concentrations of tumor necrosis factor-alpha and monocyte chemo-attractant protein-1 in mouse serum in a dose-dependent manner. LicA inhibited the allergic reaction via inhibition of IgE-mediated LAD2 cell activation through the PLC/ERK/STAT3 pathway.