Abstract
Allergy is an immune dysfunction caused by degranulation from mast cells in the early phase and cytokine secretion in the late phase of the cell. The purpose of this study was to investigate the effects of adlay (Job's tears, Coix lachryma-jobi L. var. ma-yuen Stapf) testa against beta-hexosaminidase release as a marker of degranulation in rat basophilic leukemia (RBL)-2H3 cells. The ethyl acetate fraction from ethanolic extracts of adlay testa (ATE-EtOAc) exhibited potent inhibitory activity that suppressed degranulation from RBL-2H3 cells stimulated by 1 microM A23187. The 20%-80% EtOAc/Hex subfractions of ATE-EtOAc significantly inhibited histamine release with a IC(50) of 75-100 microg/mL. In addition, the ATE-EtOAc subfractions suppressed interleukin (IL)-4, IL-6, and tumor necrosis factor-alpha secretion in RBL-2H3 cells, indicating that adlay testa were able to inhibit cytokine secretion. In order to explore the inhibitory mechanism of adlay testa in mast cell degranulation, we examined the activation of intracellular signaling molecules. Adlay testa inhibited the phosphorylation ERK expression. Furthermore, the two major active compounds, 4-hydroxyacetophenone and p-coumaric acid, were isolated from the ATE-EtOAc subfractions. These results suggest that ATE had an inhibitory effect on allergic response via the ERK signaling transduction in RBL-2H3 cells.
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