Tripterine affect substance P-sensitized mast cell activity by regulating adhesion molecules and serine/threonine kinase pathway

Abstract

Abstract Objective: The aim of this research was to analyze the mechanism of tripterine anti-inflammatory and anti-allergic activity in the substance P sensitized mast cells. Methods: Substance P was used to sensitize P815 cells, and Agilent Scanner G2505C gene chip was used to analyze differential gene. The mechanism of tripterine anti-inflammatory and anti-allergic activity was analyzed by qPCR and flow cytometry. Results: Substance P significantly inhibited P815 viability, and significantly increased histamine concentration. Significance analysis showed substance P induced 1711 genes significantly up-regulated with fold change ≥ 2, and 2033 significantly down-regulated. The GO enrichment analysis showed the up-regulated differentially expressed genes (DEGs) significantly enriched in superoxide metabolic process and nucleocytoplasmic transport, and the down-regulated DEGs mainly enriched in phosphoinositide 3-kinase cascade and blood vessel remodeling. The KEGG pathway analysis found the up-regulated DEGs mainly enriched in RNA polymerase and Huntington’s disease, and the down-regulated DEGs mainly enriched in cell adhesion molecules and lysosome. Further research found that tripterine protected substance P- sensitized mast cell by regulating cell adhesion molecules and PI3K/AKT pathway. Conclusions: This study identified some key genes and pathways closely related with sensitized mast cell, and tripterine affected substance P- sensitized cell by adhesion molecules and PI3K/AKT pathway.