Fig. 4.

DMO-CAP activates the interferon response by stimulating the Nrf2/ARE pathway to up-regulate the expression of HO-1. a Nrf2 DNA binding activity was analyzed in HEK293T-17 cells co-transfected with pGL4.37 [luc2P/ARE/Hygro]/pAP-1-Luc/pNF-κB-Luc and pRL-SV40 vector, the results were presented as Nrf2 DNA binding activity relative to its basal levels in mock 293 T. **P < 0.01 versus Mock. b DMO-CAP promoted Nrf2 nuclear transcription. RAW264.7 cells were infected with IAV A/FM1/1947 (0.2 MOI) for 2 h and treated with 50 μM DMO-CAP for another 3 h. The total amount of cellular, cytoplasmic and nuclear Nrf2 protein were analyzed by Western blot. c DMO-CAP activated the phosphorylation of p38 MAPK, JNK MAPK and ERK MAPK. RAW264.7 cells were infected with IAV A/FM1/1947 (0.2 MOI) and treated with 50μΜ DMO-CAP for 15 min and then phospho-p38、phospho-JNK and phospho-ERK proteins were valued by Western blot. d RAW264.7 cells were infected with IAV A/FM1/1947 (0.2 MOI) for 2 h, followed by treating with or without DMO-CAP (50μΜ or 25μΜ). The mRNA level of IFN-α and IFN-β were detected by qRT-PCR assay. **P < 0.01 versus Mock. e RAW264.7 cells were infected with IAV A/FM1/1947 (0.2 MOI) for 2 h and the protein levels of ISGs were measured by Western blot after treatment with DMO-CAP for 24 h