IgE, COX-2, and IL-4 are Expressed by DEHP through p38 MAPK and Suppressed by Plant Glycoprotein (75 kDa) in ICR Mice

The aim of the present study was to evaluate the inhibitory effect of glycoprotein isolated from Cudrania tricuspidata Bureau (CTB glycoprotein) on di(2-ethylhexyl) phthalate (DEHP)-induced allergic inflammatory response in mice. We evaluated the activity of beta-hexosaminidase, expression of cyclooxygenase (COX)-2, p38 mitogen-activated protein kinase (MAPK), and activator protein (AP)-1, and production of immunoglobulin (Ig)E and interleukin (IL)-4 in DEHP-treated RBL-2H3 cells and ICR mice. Our results revealed that the CTB glycoprotein inhibited the activity of beta-hexosaminidase and production of IgE and IL-4 in serum from DEHP-treated mice. We also found that the CTB glycoprotein reduced arachidonic acid release, COX-2 expression, and AP-1 transcriptional activation through p38 MAPK phosphorylation in DEHP-treated RBL-2H3 cells. The activation of AP-1 was completely blocked by treatment with p38 MAPK inhibitor (SKF86002). The results from these experiments indicate that CTB glycoprotein effectively protects against the allergic inflammation response, mainly through downregulation of MAPK/AP-1 in the mast cell degranulation stage. In conclusion, we suggest that the CTB glycoprotein may be one component of health supplements for the prevention of allergic inflammation.