Fig. 4.

Sinensetin inhibited influenza A virus-induced activation of NF-κB and MAPK signalings. a-b NF-κB reporter stable cell line HEK293 cells were stimulated with TNF-α (20 ng/mL) (a) or influenza virus A/PR/8/34 (H1N1) (MOI = 0.1) (b) in the presence or in the absence of sinensetin (0, 30, 60,120 μg/mL). After 24 h incubation, cells were lysed for luciferase activity determination. c Immunoblot analysis of phosphorylated-P65, phosphorylated-ERK1/2, phosphorylated-P38 and phosphorylated-AKT in influenza virus A/PR/8/34 (H1N1)-infected A549 cells with or without sinensetin (0, 30, 60, 120 μg/mL) treatment. GAPDH was used as internal control. d Indicated phosphorylated protein band intensities were quantified by ImageJ software. Data are expressed as mean ± SEM of three independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001 compared to influenza virus-infected alone