Deep-sea-derived viridicatol relieves allergic response by suppressing MAPK and JAK-STAT signalling pathways of RBL-2H3 cells

Our previous studies reported that viridicatol isolated from the deep-sea-derived fungus Penicillium griseofulvum could regulate the stabilisation of mast cells to relieve food allergy. To understand the molecular role of viridicatol in stabilising mast cells, transcriptomes of viridicatol-treated RBL-2H3 cells were analysed by RNA-sequencing. There were 128 differentially expressed genes in activated RBL-2H3 cells with or without viridicatol treatment. The mast cell activation-related genes were significantly reduced by treatment with viridicatol through RT-qPCR analysis. Moreover, Kyoto Encyclopedia of Genes and Genomes enrichment analysis indicated that viridicatol was important in mast cell stabilisation by affecting MAPK and JAK-STAT signalling pathways. Additionally, molecular docking and western blot analysis revealed that the phosphorylated JNK, ERK, P38, and STAT6 proteins were inhibited by viridicatol. Taken together, viridicatol has the potential to be used as a new type of anti-food allergic functional material via controlling MAPK and JAK-STAT signalling pathways of mast cells.

Automated summary

Our previous studies showed that viridicatol from the deep-sea-derived fungus Penicillium griseofulvum can regulate mast cell stabilization and relieve food allergy. To understand the molecular mechanisms, transcriptomes of viridicatol-treated RBL-2H3 cells were analyzed. Differentially expressed genes and enrichment analysis indicated that viridicatol played a significant role in mast cell stabilization by affecting MAPK and JAK-STAT signaling pathways.