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|dc.description.abstract||Cudrania tricuspidata fruit extract contains a rich source of prenylated flavonoids with potential antiatherosclerotic, hepatoprotective, and anti-inflammatory properties. However, the effect of C. tricuspidata fruit extracts and its active compounds on the high-affinity IgE receptor (FceRI)-mediated signaling remains unknown. In the present study, the effect of methanol extract from the fruits of C. tricuspidata (MFC) and its active compound, 5,7,3',4'-tetrahydroxy-6,8-diprenylisoflavone (THDPI), on FceRI-mediated signaling in mast cells was investigated. MFC and THDPI suppressed mast cell degranulation and Ca2+ influx. MFC also interfered with IgE-FceRI interaction and decreased FceRI beta mRNA expression in mast cells. Furthermore, MFC and THDPI inhibited the phosphorylation of Syk, LAT, and PLC gamma and F-actin redistribution. These results indicate that MFC and its active compound, THDPI, inhibit mast cell activation through the inhibition of FceRI-mediated Syk activation, suggesting a therapeutic potential for controlling mast cell activation in inflammatory and/or allergic processes.||-|
|dc.publisher||Journal of agricultural and food chemistry||-|
|dc.title||Effects of Cudrania tricuspidata Fruit Extract and Its Active Compound, 5,7,3 ',4 '-Tetrahydroxy-6,8-diprenylisoflavone, on the High-Affinity IgE Receptor-Mediated Activation of Syk in Mast Cells||-|
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