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

MAPK/ERK通路 斯达 肥大细胞 转录组 免疫印迹 生物 信号转导 p38丝裂原活化蛋白激酶 基因 JAK-STAT信号通路 刺猬信号通路 细胞生物学 分子生物学 基因表达 免疫学 遗传学 车站3 酪氨酸激酶
作者
Yan Liu,Zhendan Shu,Yan Li,Huiying Chen,Hong Liu,Xian‐Wen Yang,Guang‐Ming Liu,Qingmei Liu
出处
期刊:Food and Agricultural Immunology [Taylor & Francis]
卷期号:34 (1) 被引量:5
标识
DOI:10.1080/09540105.2023.2207791
摘要

ABSTRACTOur 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.
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