Figure 7.

Syk affinitive compounds in PLE attenuated allergic inflammation by synergistically targeting on Syk in DNP-IgE/BSA-induced RBL-2H3 cell. (A) (a) Representative photomicrographs (×200) of Syk expression in RBL-2H3 cells and (b) their relative fluorescence intensities as determined by immunofluorescence staining (n = 3). (B) The expression of Syk in DNP-IgE/BSA-induced RBL-2H3 cells with Mix of Syk affinitive compounds co-treated with Syk inhibitor detected by WB (n = 5). (C) (a) Representative photomicrographs of (×200) p-Syk in RBL-2H3 cells and (b) their relative fluorescence intensities as determined by immunofluorescence staining (n = 3). (D) The expression of p-Syk in DNP-IgE/BSA-induced RBL-2H3 cells with Mix of Syk affinitive compounds co-treated with Syk inhibitor detected by WB (n = 5). (E–J) The expression of PKC, p-PKC, p65, p-p65, cPLA₂, and p-cPLA₂ in DNP-IgE/BSA-induced RBL-2H3 cells with Mix of Syk affinitive compounds treatment with the Syk inhibitor detected by WB (n = 5). (K–P) The expression of Syk and p-Syk in DNP-IgE/BSA-induced RBL-2H3 cells with Mix of Syk affinitive compounds co-treated with PKC, NF-κB and cPLA₂ inhibitors detected by WB (n = 5). Data were shown as mean ± SEM. ^##P < 0.01 vs control group; *P < 0.05 and **P < 0.01 vs model group.