Fig 2: Potential interaction between signaling pathways of AMPK/Sirt1 and Nrf2/HO-1. The 16HBE cells were treated as described in the method. The protein level was detected by western blot. (A) The levels of p-AMPK, Sirt1, Nrf2 and HO-1. ## p < .01, compared with the siControl + Pts group. (B) p-AMPK, Sirt1, Nrf2 and HO-1 levels. **p < .01, compared with the Control group. ## p < .01, compared with the Pts group. (C) Sirt1, Nrf2 and HO-1 levels. **p < .01, compared with Control group. ## p < .01, compared with the Pts group. (D) Nrf2 and HO-1 levels. **p < .01, compared with Control group. ## p < .01, compared with the Pts group. Each data value represents mean ± SD. AMPK, adenosine 5'-monophosphate-activated protein kinase; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; HO-1, Heme oxygenase-1; Nrf2, nuclear factor-E2-related factor 2; Pts, Pterostilbene

Fig 3: Pterostilbene activates AMPK/Sirt1 pathway. (A, B) Protein levels in lung tissues of mice were detected by western blot. (C) Detection of p-AMPK protein expressioninmice by immunofluorescence. (D) P-AMPK expression in mice was detected by immunohistochemical staining. (E, F) Protein levels in 16HBE cells were measured with Western blot. (H) The p-AMPK in 16HBE cells was detected by immunofluorescence. All data were expressed as mean ± SD. *p < .05, **p < .01, compared with the Control group. # p < .05, ## p < .01, compared with the OVA group or LPS group. AMPK, adenosine 5'-monophosphate-activated protein kinase; DAPI, 4',6-diamidino-2-phenylindole; LPS, lipopolysaccharide; OVA, ovalbumin