IgE-Induced Mast Cell Activation Is Suppressed by Dihydromyricetin through the Inhibition of NF-κB Signaling Pathway

Molecules

Tsong-Min Chang¹  Huey-Chun Huang²  Ting-Ya Yang²  Tzu-Chih Hsiao³ 

[1] Department of Applied Cosmetology, Hungkuang University, Taichung 433304, Taiwan;Department of Medical Laboratory Science and Biotechnology, College of Medicine, China Medical University, Taichung 404333, Taiwan;Juwenlee Cosmetics Technology Center, LUO LI-FEN Group, Zhangzhou 363105, China;

关键词: dihydromyricetin;    mast cells;    NF-κB;    tryptase;    STAT5;   

DOI  :  10.3390/molecules26133877

来源: DOAJ

【 摘 要 】

Mast cells play a crucial role in the pathogenesis of type 1 allergic reactions by binding to IgE and allergen complexes and initiating the degranulation process, releasing pro-inflammatory mediators. Recently, research has focused on finding a stable and effective anti-allergy compound to prevent or treat anaphylaxis. Dihydromyricetin (DHM) is a flavonoid compound with several pharmacological properties, including free radical scavenging, antithrombotic, anticancer, and anti-inflammatory activities. In this study, we investigated the anti-allergic inflammatory effects and the underlying molecular mechanism of DHM in the DNP-IgE-sensitized human mast cell line, KU812. The cytokine levels and mast cell degranulation assays were determined by enzyme-linked immunosorbent assay (ELISA). The possible mechanism of the DHM-mediated anti-allergic signaling pathway was analyzed by western blotting. It was found that treatment with DHM suppressed the levels of inflammatory cytokines TNF-α and IL-6 in DNP-IgE-sensitized KU812 cells. The anti-allergic inflammatory properties of DHM were mediated by inhibition of NF-κB activation. In addition, DHM suppressed the phosphorylation of signal transducer and activator of transcription 5 (STAT5) and mast cell-derived tryptase production. Our study shows that DHM could mitigate mast cell activation in allergic diseases.

【 授权许可】

Unknown