Coptis cream ethanol extract regulates degranulation caused by allergic reactions through MGPRB3/PLC/TRPV1 signaling pathway.

ETHNOPHARMACOLOGICAL RELEVANCE

The classic formulation, Coptis cream, is widely used in clinical practice to treat allergic skin conditions, including eczema and urticaria. Through extraction screening, Coptis cream extract obtained with 75% ethanol (referred to as RPTCA) demonstrated optimal anti-allergic effects. However, the underlying mechanism of its anti-allergic action remains unexplored.

AIM OF THE STUDY

To investigate the anti-allergic effects of RPTCA and to explore its possible mechanism of action.

METHODS

The anti-allergic effects of RPTCA were investigated in C48/80-induced allergy models, namely, RBL-2H3 cells in vitro and foot-swelling mouse models in vivo. The underlying mechanisms and the monomer composition of RPTCA were explored.

RESULTS

Results demonstrated that RPTCA significantly reduced C48/80-induced foot swelling, vascular permeability, mast cell count, and cytokine secretion in mice. Mechanistic analysis revealed that C48/80 activated TRPV1 and TRPV4, with TRPV1 inhibition suppressing cell degranulation. RPTCA downregulated MRGPRB3 overexpression and degranulation levels, while MRGPRB3 inhibition markedly suppressed C48/80 activation and degranulation. RPTCA also decreased PLC phosphorylation through MRGPRB3, reduced intracellular Ca and CaMKII phosphorylation, inhibited PKC phosphorylation, suppressed TRPV1 activation, and ultimately limited mast cell degranulation. Furthermore, RPTCA downregulated NF-κB and ERK/JNK signaling pathways, inhibiting inflammatory factor release. The component analysis identified nine main components in RPTCA, each capable of inhibiting cell degranulation.

CONCLUSIONS

RPTCA inhibits TRPV1 activation and reduces cell degranulation through the PLC/Ca/PKC pathway, while also suppressing the secretion of inflammatory factors through the NF-κB signaling pathway and ERK/JNK proteins.