Fig. 1.

Reduction of AMPK activity in ablation and infarction (A/I) kidney cortex. Each immunoblot was sequentially probed with three antibodies to p-AMPKα (Thr¹⁷²), AMPKα1, and anti-GAPDH, respectively. AMPK phosphorylation at threonine-172 (Thr¹⁷²) in the α-subunit is a key regulator of AMPK activation and is an established marker for activated AMPK. The anti-AMPKα antibody recognizes total AMPKα protein. Anti-GAPDH or anti-β-actin antibodies were used for normalization of sample loading and transfer efficiency. AMPK activity tends to decrease in the A/I kidney relative to the normal kidney by day 3 after A/I (A), but is not significant. This decrease becomes significant by day 5 (B) after the injury and progresses in day 7 (C). Respective graphs are below the immunoblots. Both p-AMPK and the p-AMPK/AMPK ratio yielded similar results. Data are expressed as means ± SE. *P < 0.01 vs. normal; n = 3 or 4.