Fig. 7

AMPK activation is required for inhibiting NF-κB p65 translocation. Compound C reverses the effects of AICAR to suppress CFA-induced NF-κB p65 translocation in CX3CR1-GFP mice. After a pre-treatment of Compound C (80 μg/20 μl), mice were treated with AICAR (15 μg/20 μl). Skin tissues from CX3CR1-GFP mice were collected at 2 h after AICAR treatment for immunofluorescence. a AICAR inhibited the CFA-induced NF-κB translocation from the cytosol to the nucleus, as demonstrated by the immunofluorescence of NF-κB p65 in CX3CR1-GFP-marked macrophage cells. Scale bars represent 50 μm. The same experimental results were repeated in four mice of each group. The bottom line of the panels shows the merged profiles of the fluorescent intensity of CX3CR1-GFP, NF-κB p65, and DAPI signals along the lines drawn through the axis of CX3CR1-GFP-positive macrophage cells. b Quantification for CX3CR1-GFP protein level of skin tissues. c Quantification for CX3CR1-GFP macrophages with p65 translocation of a. Non-paired Student’s t test revealed a significant difference at *P < 0.05 vs. Control group, ^#P < 0.01 vs. CFA + VEH group, and ^&P < 0.05 vs. CFA + AICAR group, (n = 4 mice/group). d The panels are images showing double-labeled cells in CX3CR1-GFP mice (after CFA injection at day 4) with CD68 and DAPI. The abbreviations used here are VEH (vehicle of AICAR) and CC (Compound C)