Conclusion
Saposhnikovia divaricata could inhibit IgE-induced degranulation of mast cells, providing a scientific basis for further research and clinical applications of SD in TIA treatment.
Methods
The effective components and action targets of SD were screened using TCMSP database, and allergy-related targets of SD were predicted using GeneCards and OMIM database. The obtained target intersections were imported into David database for GO analysis, and used R software to perform KEGG analysis. The RBL-2H3 cells sensitised by DNP-IgE/DNP-BSA were treated with different concentrations of SD (root decoction, 0.5, 1, and 2 mg/mL), prim-O-glucosylcimifugin (POG, 10, 40, and 80 μg/mL) and the positive control drug-ketotifen fumarate (KF, 30 μM) for 12 h, then subjected to cell degranulation and qPCR analysis.
Objective
This study evaluates the treatment and molecular mechanisms of SD against TIA. Materials and
Results
Eighteen active compounds of SD and 38 intersection targets were obtained: TIA-related signal pathways mainly include calcium signal pathway, PI3K-Akt signal pathway and MAPK signal pathway. Taking the β-Hex release rate of the model group as the base, the release rate of SD and POG in high dose groups were 43.79% and 57.01%, respectively, which were significantly lower than model group (p < 0.01), and significantly lower than KF group (63.83%, p < 0.01, p < 0.05). SD and POG could down-regulate the expression of related proteins in the Lyn/Syk, PI3K/AKT and MAPK signalling pathways.