FIGURE 4.

The effect of resveratrol on AMPK phosphorylation is mediated by LKB1 without cross-talk between AMPK and Akt, and its effect on NFAT-dependent transcription is mainly dependent on AMPK not Akt. A-C, representative immunoblots of cellular extracts from mouse embryonic fibroblasts (MEFs) treated with ethanol (Control) or 100 μm resveratrol (Resv) for 1 h, blotted with anti-phospho-α-AMPK (T172), anti-α-AMPK, anti-phospho-Akt (S473), and anti-Akt antibodies. A, wild-type (WT) and LKB1-null MEFs; B, WT and AMPKα1/α2-null MEFs; and C, WT and Akt1/2-null MEFs were utilized (n = 3). D and E, AMPKα1/α2-null and Akt1/2-null MEFs with their respective WT MEFs were infected with Ad.NFAT-Luc-Promoter adenovirus and then treated with ethanol (Control) or 100 μm Resv for 1 h. NFAT-dependent transcription measured from cellular extracts is presented as a percentage (%) compared with control-treated, where values are means ± S.E. D,^*, p < 0.01 versus WT control-treated; #, p < 0.05 versus AMPKα1/α2-null control-treated (n = 4-6), assessed by two-tailed Mann-Whitney test. E,^*, p < 0.001 versus WT control-treated; #, p < 0.001 versus Akt1/2-null control-treated (n = 3), assessed by Student's unpaired two-tailed t test.