Myricetin alleviated immunologic contact urticaria and mast cell degranulation via the PI3K/Akt/NF‐κB pathway

Abstract

AbstractImmunologic contact urticaria (ICU) is characterized by the wheal and flare reaction from direct contact with a chemical or protein agent, which involves a type I hypersensitivity mediated by allergen‐specific immunoglobulin E (sIgE). Myricetin (Myr), a bioactive flavonoid, exhibits antiinflammatory activities. Our results showed that treatment with Myr could alleviate ICU symptoms, including a decrease in the number of wheals and scratching, and inhibit ear swelling in the IgE/DNFB‐induced mice. The serum level of IgE, histamine, interleukin (IL)‐4, TNF‐α, and MCP‐1 were reduced in Myr‐treated mice. Myr also attenuated mast cells (MCs) degranulation and H‐PGDS, TSLP, IL‐33, PI3K, Akt, and NF‐κB mRNA levels in ICU model. The IgE‐mediated anaphylaxis mouse models demonstrated anti‐allergic effects of Myr. In vitro analysis showed that Myr reduced IgE‐induced calcium (Ca2+) influx, suppressed degranulation, and chemokine release in LAD2 cells (human primary mast cells). Myr can significantly inhibited PLCγ1, Akt, NF‐κB, and p38 phosphorylation. In conclusion, the study demonstrated that Myr alleviate ICU symptoms and inhibit mast cell activation via PI3K/Akt/NF‐κB signal pathway.