摘要：IgE-mediated mast cell activation is critical for development of allergic inflammation. We have recently found that selinidin, one of the coumarin derivatives isolated from Angelica keiskei , attenuates mast cell degranulation following engagement of the high-affinity receptor for IgE (FcεRI) with IgE and antigen. In the present study, we investigated the effects of selinidin on intracellular signaling and mast cell activation employing bone marrow-derived mast cells. Here, we report that selinidin attenuates the release of β-hexosaminidase, synthesis of leukotriene C4, and production of tumor necrosis factor-α without affecting IgE-FcεRI binding. Furthermore, biochemical analyses of the FcεRI-mediated signaling pathway demonstrated that selinidin decreases phosphorylation of phospholipase C-γ1, p38 mitogen-activated protein kinase, and IκB-α upon FcεRI stimulation. These results suggest that this compound suppresses IgE-mediated mast cell activation by inhibiting multiple steps of FcεRI-dependent signaling pathways and would be beneficial for the prevention of allergic inflammation.
关键词：IgE;mast cell;high-affinity receptor for IgE (FcεRI);selinidin;degranulation;cytokine production
