Fig. 6

SS2-induced transactivation of EGFR contributes to the neuroinflammation via MAPK-ERK1/2 and NF-κB signaling pathways. a, b NF-κB inhibitors BAY11-7082 or CAY10657 and the ERK1/2 inhibitor U0126 dose-dependently inhibited SS2-induced upregulation of IL-6 and MCP-1. c SC19 infection of hBMEC induced an obvious phosphorylation of p65 subunit, as well as the degradation of IκBα. d SC19 infection of hBMEC induced obvious activation of ERK1/2. e, f EGFR-selective inhibitor AG1478 could significantly decrease the SC19-induced NF-κB signaling (including p65 phosphorylation and IκBα degradation), as well as ERK1/2 phosphorylation. g Blockage of ERK1/2 signaling by U0126 did not affect SS2-induced p65 phosphorylation and IκBα degradation. h Fluorescence microscopy of SS2-induced p65 subunit translocation to the nucleus in hBMEC with pretreatment of AG1478 (5 μM), U0126 (5 μM), or BAY-11-7082 (5 μM). Cells were incubated with anti-p65 antibody and visualized with a FITC-labeled goat anti-mouse IgG antibody. Scale bar = 100 μm