Fig. 7
Activation of AMPKα by 5-MF has a role in the inhibition of NF-kB and P38 MAPK signaling pathways. A Two days prior to the 5LD50 of H1N1 virus infection, mice were intragastrically administered 5-MF alone or in combination with compound C (20 mg·kg−1·d−1) intraperitoneal injection, and the mice in the H1N1 + 5-MF + compound C group were intraperitoneally injected with compound C for 30 min before 5-MF administration. On day 7 p.i., histopathological changes of the lungs were examined by H&E staining. B Lung injury score was evaluated according to the lung histopathology changes. C–H After pretreatment with compound C (10 μM) for 1 h, H1N1 virus-infected A549 cells were incubated with 5-MF for 24 h. C Western blotting was performed to detect the phosphorylation of IKBα, P65, and P38. D The relative protein band intensities of P-IKBα, P-P65, and P-P38 were quantitated using ImageJ software. E Luminex assay for proinflammatory mediators (IL-6, CXCL10, and TNF-α) in culture supernatants. F Western blotting was performed to determine the expression of COX-2. G The relative protein band intensity of COX-2 was quantitated using ImageJ software. H ELISA assay for PGE2 in culture supernatants. ##p < 0.01, ###p < 0.001 relative to the control group; *p < 0.05, **p < 0.01, ***p < 0.001 relative to the virus group; &p < 0.05 relative to the H1N1 virus + 5-MF (40 mg·kg−1·d−1); δp < 0.05, δδp < 0.01 relative to the H1N1 virus + 5-MF (20 μM) group; ξp < 0.05, ξξp < 0.01, ξξξp < 0.001 relative to the H1N1 virus + 5-MF (30 μM) group