Fig 6.

S0 and S3 inhibited the activation of the IKK and ERK/p38 MAPK pathways, and an oxidant and IKK, ERK, and p38 activators antagonized the anti-IAV activities of S0 and S3. (A) S0 and S3 inhibited the activation of the IKK and ERK/p38 MAPK pathways after IAV infection, as determined by Western blotting. A549 cells were infected and treated or not with ribavirin, S0, and S3. After 24 h, the cells were collected and subjected to Western blotting. In noninfected or infected A549 cells, 0.5% DMSO was used as a BG or NC, respectively, and ribavirin was used as a PC (MOI = 0.001; incubation time, 24 h). The zones and average gray values of each band were detected and quantified with BandScan 5.0 software, the multiplication product of the zone area and the average gray value was calculated, and the results were expressed as the ratios of the target genes to β-actin. (B) An oxidant and IKK, ERK, and p38 activators antagonized the anti-IAV activities of S0 and S3. A549 cells were infected (MOI = 0.001) and treated or not with ribavirin, S0, or S3; the cells were simultaneously treated or not with H₂O₂ (100 μM), LPS (10 μM), EGF (100 ng/ml), and anisomycin (10 μM). After 24 h, the antiviral activity (cell viability) was determined by the SRB method. The concentrations of S0, S3, and ribavirin were 100, 80, and 200 μM, respectively. The data are expressed as the means ± SD of three independent experiments. *, P < 0.05, and **, P < 0.01 versus the NC (A) or virus (V)-plus-drug control (B).