Paeoniflorin inhibits degranulation of mast cells through suppressing the cGAS/STING signaling pathway

Allergic rhinitis is an allergic disease that affects the nasal mucosa, and its incidence has been increasing significantly in recent years. Paeoniflorin (PF) is the main chemical component of total glucosides of paeony and is reported to have an excellent effect on anti-allergic inflammation. In this study, we aimed to investigate the mechanism of PF regulating the degranulation of mast cells induced by dinitrophenol (DNP)-human serum albumin (DNP-HSA).

The effect of PF on the degranulation of mast cells was evaluated through the measurement of histamine, β-hexosaminidase, and intracellular calcium level, and the signaling pathway was screened through western blot assay and molecular docking.

The results showed that PF treatment reduced the release of histamine and β-hexosaminidase, and reduced the intracellular calcium level in mast cells with DNP-HSA treatment. In addition, PF downregulated the protein levels of cGAS and STING to inactivate the cGAS/STING signaling pathway, in which the inhibitory effects of PF on mast cells were reversed by 5,6-imethylxanthenone-4-acetic acid (DMXAA, a STING agonist).

In conclusion, PF inhibits degranulation of mast cells through the cGAS/STING signaling pathway, which provides a theoretical basis for the application of PF in allergic rhinitis therapy.